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Limnological Papers     Open Access   (Followers: 1)
Lipid Insights     Open Access   (Followers: 1)
Lipid Technology     Hybrid Journal   (Followers: 2)
Lipids     Hybrid Journal   (Followers: 1)
Lipids in Health and Disease     Open Access  
Luminescence     Hybrid Journal   (Followers: 1)
mAbs     Full-text available via subscription   (Followers: 4)
Macromolecular Bioscience     Hybrid Journal   (Followers: 1)
Macromolecular Reaction Engineering     Hybrid Journal  
Madroño     Full-text available via subscription  
Malacologia     Full-text available via subscription   (Followers: 1)
Malacologica Bohemoslovaca     Open Access  
Malawi Journal of Science and Technology     Open Access   (Followers: 2)
Mammal Review     Hybrid Journal   (Followers: 5)
Mammal Study     Full-text available via subscription   (Followers: 1)
Mammalian Biology - Zeitschrift für Säugetierkunde     Hybrid Journal   (Followers: 5)
Mammalian Genome     Hybrid Journal   (Followers: 3)
Mammalian Species     Full-text available via subscription   (Followers: 2)
Manufacturing Engineer     Hybrid Journal   (Followers: 3)
Marine Biodiversity     Hybrid Journal   (Followers: 10)
Marine Biodiversity Records     Hybrid Journal   (Followers: 7)
Marine Biology     Hybrid Journal   (Followers: 199)
Marine Biotechnology     Hybrid Journal   (Followers: 6)
Marine Mammal Science     Hybrid Journal   (Followers: 6)
Materials Science and Engineering: C     Hybrid Journal   (Followers: 18)
Materials Technology: Advanced Performance Materials     Hybrid Journal   (Followers: 6)
Mathematical Biosciences     Hybrid Journal   (Followers: 3)
Mathematical Medicine and Biology: A Journal of the IMA     Hybrid Journal   (Followers: 2)
Mathematical Physics, Analysis and Geometry     Hybrid Journal   (Followers: 1)
Mathematical Problems in Engineering     Open Access   (Followers: 3)
Matrix Biology     Hybrid Journal  
Médecine Nucléaire     Full-text available via subscription  
mBio     Open Access   (Followers: 3)
Mechanisms of Ageing and Development     Hybrid Journal   (Followers: 2)
Mechanisms of Development     Hybrid Journal   (Followers: 4)
médecine/sciences     Full-text available via subscription   (Followers: 1)
Medical and Biological Engineering and Computing     Hybrid Journal   (Followers: 2)
Medical and Biological Sciences     Open Access  
Medical Engineering & Physics     Hybrid Journal   (Followers: 9)
Membrane Protein Transport     Full-text available via subscription   (Followers: 3)
Memoirs of the Association of Australasian Palaeontologists     Full-text available via subscription   (Followers: 2)
Metabolic Engineering     Hybrid Journal   (Followers: 8)
Metabolites     Open Access   (Followers: 1)
Metabolomics     Hybrid Journal   (Followers: 5)
Metallomics     Full-text available via subscription  
Methods     Hybrid Journal   (Followers: 11)
Methods in Cell Biology     Full-text available via subscription   (Followers: 6)
Methods in Cell Science     Hybrid Journal   (Followers: 3)
Methods in Ecology and Evolution     Partially Free   (Followers: 16)
Micologia Aplicada Internacional     Open Access  
Microarrays     Open Access  
Micron     Hybrid Journal  
Mitochondrial DNA     Hybrid Journal   (Followers: 3)
Mitochondrion     Hybrid Journal   (Followers: 3)
Modelling and Simulation in Engineering     Open Access   (Followers: 4)
Modelling and Simulation in Materials Science and Engineering     Hybrid Journal   (Followers: 7)
Modern Chemotherapy     Open Access  
Molecular & Cellular Proteomics     Full-text available via subscription   (Followers: 11)
Molecular & Cellular Toxicology     Hybrid Journal   (Followers: 2)
Molecular and Biochemical Parasitology     Hybrid Journal   (Followers: 2)
Molecular and Cellular Biochemistry     Hybrid Journal   (Followers: 4)
Molecular and Cellular Biology     Full-text available via subscription   (Followers: 19)
Molecular Based Mathematical Biology     Open Access  
Molecular Biology     Hybrid Journal   (Followers: 10)
Molecular Biology and Evolution     Hybrid Journal   (Followers: 220)
Molecular Biology International     Open Access   (Followers: 3)
Molecular Biology of the Cell     Partially Free   (Followers: 17)
Molecular Biology Reports     Hybrid Journal   (Followers: 4)
Molecular Brain     Open Access   (Followers: 2)
Molecular Breeding     Hybrid Journal   (Followers: 6)
Molecular Cell     Full-text available via subscription   (Followers: 38)
Molecular Ecology     Hybrid Journal   (Followers: 23)
Molecular Ecology Resources     Hybrid Journal   (Followers: 10)
Molecular Genetics and Metabolism     Hybrid Journal   (Followers: 6)
Molecular Immunology     Hybrid Journal   (Followers: 11)
Molecular Membrane Biology     Hybrid Journal   (Followers: 1)
Molecular Neurobiology     Hybrid Journal   (Followers: 3)
Molecular Pain     Open Access  
Molecular Plant-Microbe Interactions     Partially Free   (Followers: 5)
Molecular Reproduction & Development     Hybrid Journal   (Followers: 7)
Molecular Therapy - Nucleic Acids     Open Access  
Molecules and Cells     Hybrid Journal   (Followers: 1)
Momona Ethiopian Journal of Science     Open Access   (Followers: 3)
Monoclonal Antibodies in Immunodiagnosis and Immunotherapy     Hybrid Journal  
Monographs of the Western North American Naturalist     Full-text available via subscription   (Followers: 1)
Moscow University Physics Bulletin     Hybrid Journal  
Movement Ecology     Open Access   (Followers: 4)
Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis     Hybrid Journal   (Followers: 2)
Mutation Research/Genetic Toxicology and Environmental Mutagenesis     Hybrid Journal   (Followers: 7)
Mutation Research/Reviews in Mutation Research     Hybrid Journal   (Followers: 4)
Mycological Progress     Hybrid Journal   (Followers: 1)
Mycopathologia     Hybrid Journal   (Followers: 1)
Mycorrhiza     Hybrid Journal   (Followers: 5)
Mycoscience     Hybrid Journal   (Followers: 1)
Mycotoxin Research     Hybrid Journal   (Followers: 4)
NAMMCO Scientific Publications     Open Access  
Nano Reviews     Open Access   (Followers: 17)
Nano Today     Hybrid Journal   (Followers: 18)
Nanoscale Research Letters     Open Access   (Followers: 4)
Natural Hazards     Hybrid Journal   (Followers: 310)

  First | 6 7 8 9 10 11 12 13 | Last

Journal Cover   Biochemistry and Cell Biology
  [SJR: 1.331]   [H-I: 70]   [10 followers]  Follow
   Full-text available via subscription Subscription journal
   ISSN (Print) 0829-8211 - ISSN (Online) 1208-6002
   Published by NRC Research Press Homepage  [19 journals]
  • Note of appreciation / Note de reconnaissance
    • Pages: iii - iv
      Abstract: Biochemistry and Cell Biology, Volume 93, Issue 1, Page iii-iv, February 2015.
      Citation: Biochemistry and Cell Biology
      PubDate: Mon, 26 Jan 2015 11:13:18 GMT
      DOI: 10.1139/bcb-2015-0004
  • Corrigendum: Acid-base transport in pancreatic cancer: Molecular
           mechanisms and clinical potential
    • Authors: Su Chii Kong, Andrea Giannuzzo, Ivana Novak, Stine Falsig Pedersen
      Pages: 1 - 1
      Abstract: Biochemistry and Cell Biology, e-First Articles.
      Citation: Biochemistry and Cell Biology
      PubDate: Thu, 05 Mar 2015 17:31:39 GMT
      DOI: 10.1139/bcb-2015-0026
  • My road to alternative splicing control: from simple paths to loops and
    • Authors: Benoit Chabot
      Pages: 1 - 9
      Abstract: Biochemistry and Cell Biology, e-First Articles. With the functional importance of alternative splicing being validated in nearly every mammalian biological system and implicated in many human diseases, it is now crucial to identify the molecular programs that control the production of splice variants. In this article, I will survey how our knowledge of the basic principles of alternative splicing control evolved over the last 25 years. I will also describe how investigation of the splicing control of an apoptotic regulator led us to identify novel effectors and revealed the existence of converging pathways linking splicing decisions to DNA damage. Finally, I will review how our efforts at developing tools designed to monitor and redirect splicing helped assess the impact of misregulated splicing in cancer.
      Citation: Biochemistry and Cell Biology
      PubDate: Thu, 12 Feb 2015 08:00:00 GMT
      DOI: 10.1139/bcb-2014-0161
  • Chronic activation of pattern recognition receptors suppresses brown
           adipogenesis of multipotent mesodermal stem cells and brown pre-adipocytes
    • Authors: Jiyoung Bae, Jiangang Chen, Ling Zhao
      Pages: 1 - 11
      Abstract: Biochemistry and Cell Biology, e-First Articles. Brown adipose tissue (BAT) holds promise to combat obesity through energy-spending, non-shivering thermogenesis. Understanding of regulation of BAT development can lead to novel strategies to increase BAT mass and function for obesity treatment and prevention. Here, we report the effects of chronic activation of PRR on brown adipogenesis of multipotent mesodermal stem C3H10T1/2 cells and immortalized brown pre-adipocytes from the classical interscapular BAT of mice. Activation of NOD1, TLR4, or TLR2 by their respective synthetic ligand suppressed brown marker gene expression and lipid accumulation during differentiation of brown-like adipocytes of C3H10T1/2. Activation of the PRR only during the commitment was sufficient to suppress the differentiation. PRR activation suppressed PGC-1α mRNA, but induced PRDM16 mRNA at the commitment. Consistently, PRR activation suppressed the differentiation of immortalized brown pre-adipocytes. Activation of PRR induced NF-κB activation in both cells, which correlated with their abilities to suppress PPARγ transactivation, a critical event for brown adipogenesis. Taken together, our results demonstrate that chronic PRR activation suppressed brown adipogenesis of multipotent mesodermal stem cells and brown pre-adipocytes, possibly through suppression of PPARγ transactivation. The results suggest that anti- inflammatory therapies targeting PRRs may be beneficial for the BAT development.
      Citation: Biochemistry and Cell Biology
      PubDate: Thu, 05 Feb 2015 08:00:00 GMT
      DOI: 10.1139/bcb-2014-0139
  • On the mechanism of phosphoenolpyruvate synthetase (PEPs) and its
           inhibition by sodium fluoride: potential magnesium and aluminum fluoride
           complexes of phosphoryl transfer
    • Authors: Nicole E. McCormick, David L. Jakeman
      Pages: 1 - 5
      Abstract: Biochemistry and Cell Biology, e-First Articles. Phosphoenolpyruvate synthase (PEPs) catalyzes the conversion of pyruvate to phosphoenolpyruvate (PEP) using a two-step mechanism invoking a phosphorylated-His intermediate. Formation of PEP is an initial step in gluconeogenesis, and PEPs is essential for growth of Escherichia coli on 3-carbon sources such as pyruvate. The production of PEPs has also been linked to bacterial virulence and antibiotic resistance. As such, PEPs is of interest as a target for antibiotic development, and initial investigations of PEPs have indicated inhibition by sodium fluoride. Similar inhibition has been observed in a variety of phospho-transfer enzymes through the formation of metal fluoride complexes within the active site. Herein we quantify the inhibitory capacity of sodium fluoride through a coupled spectrophotometric assay. The observed inhibition provides indirect evidence for the formation of a MgF3− complex within the enzyme active site and insight into the phospho-transfer mechanism of PEPs. The effect of AlCl3 on PEPs enzyme activity was also assessed and found to decrease substrate binding and turnover.
      Citation: Biochemistry and Cell Biology
      PubDate: Mon, 26 Jan 2015 08:00:00 GMT
      DOI: 10.1139/bcb-2014-0153
  • Cyclophilin D disruption attenuates lipopolysaccharide-induced
           inflammatory response in primary mouse macrophages
    • Authors: Janos Priber, Fruzsina Fonai, Peter Balazs Jakus, Boglarka Racz, Christos Chinopoulos, Laszlo Tretter, Ferenc Gallyas, Balazs Sumegi, Balazs Veres
      Pages: 1 - 10
      Abstract: Biochemistry and Cell Biology, e-First Articles. According to recent results, various mitochondrial processes can actively regulate the immune response. In the present report, we studied whether mitochondrial permeability transition (mPT) has such a role. To this end, we compared bacterial lipopolysaccharide (LPS)-induced inflammatory response in cyclophilin D (CypD) knock-out and wild-type mouse resident peritoneal macrophages. CypD is a regulator of mPT; therefore, mPT is damaged in CypD−/− cells. We chose this genetic modification-based model because the mPT inhibitor cyclosporine A regulates inflammatory processes by several pathways unrelated to the mitochondria. The LPS increased mitochondrial depolarisation, cellular and mitochondrial reactive oxygen species production, nuclear factor-κB activation, and nitrite- and tumour necrosis factor α accumulation in wild-type cells, but these changes were diminished or absent in the CypD-deficient macrophages. Additionally, LPS enhanced Akt phosphorylation/activation as well as FOXO1 and FOXO3a phosphorylation/inactivation both in wild-type and CypD−/− cells. However, Akt and FOXO phosphorylation was significantly more pronounced in CypD-deficient compared to wild-type macrophages. These results provide the first pieces of experimental evidence for the functional regulatory role of mPT in the LPS-induced early inflammatory response of macrophages.
      Citation: Biochemistry and Cell Biology
      PubDate: Fri, 23 Jan 2015 08:00:00 GMT
      DOI: 10.1139/bcb-2014-0120
  • Epigenetics in idiopathic pulmonary fibrosis
    • Authors: Argyrios Tzouvelekis, Naftali Kaminski
      Pages: 1 - 12
      Abstract: Biochemistry and Cell Biology, e-First Articles. Idiopathic pulmonary fibrosis (IPF) is a lethal chronic lung disorder with no effective treatment and a prognosis worse than that of lung cancer. Despite extensive research efforts, its etiology and pathogenesis still remain largely unknown. Current experimental evidence has shifted the disease paradigm from chronic inflammation towards the premise of abnormal epithelial wound repair in response to repeated epigenetic injurious stimuli in genetically predisposed individuals. Epigenetics is defined as the study of heritable changes in gene function by factors other than an individual’s DNA sequence, providing valuable information regarding adaption of genes to environmental changes. Although cancer is the most studied disease with relevance to epigenetic modifications, recent data support the idea that epigenomic alterations may lead to variable disease phenotypes, including fibroproliferative lung disorders such as IPF. This review article summarizes the latest experimental and translational epigenetic studies in the research field of chronic lung disorders, mainly focusing on IPF, highlights current methodology limitations, and underlines future directions and perspectives.
      Citation: Biochemistry and Cell Biology
      PubDate: Tue, 13 Jan 2015 08:00:00 GMT
      DOI: 10.1139/bcb-2014-0126
  • MicroRNA regulatory networks in idiopathic pulmonary fibrosis
    • Authors: Kusum V. Pandit, Jadranka Milosevic
      Pages: 1 - 9
      Abstract: Biochemistry and Cell Biology, e-First Articles. Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, and fatal scarring lung disease of unknown etiology, characterized by changes in microRNA expression. Activation of transforming growth factor (TGF-β) is a key event in the development of IPF. Recent reports have also identified epigenetic modification as an important player in the pathogenesis of IPF. In this review, we summarize the main results of studies that address the role of microRNAs in IPF and highlight the synergistic actions of these microRNAs in regulating TGF-β, the primary fibrogenic mediator. We outline epigenetic regulation of microRNAs by methylation. Functional studies identify microRNAs that alter proliferative and migratory properties of fibroblasts, and induce phenotypic changes in epithelial cells consistent with epithelial-mesenchymal transition. Though these studies were performed in isolation, we identify multiple co-operative actions after assembling the results into a network. Construction of such networks will help identify disease-propelling hubs that can be targeted for therapeutic purposes.
      Citation: Biochemistry and Cell Biology
      PubDate: Mon, 05 Jan 2015 12:51:20 GMT
      DOI: 10.1139/bcb-2014-0101
  • Deception in simplicity: Hereditary phospholamban mutations in dilated
    • Authors: Howard S. Young, Delaine K. Ceholski, Catharine A. Trieber
      Pages: 1 - 7
      Abstract: Biochemistry and Cell Biology, Volume 93, Issue 1, Page 1-7, February 2015. The sarcoplasmic reticulum (SR) calcium pump (SERCA) and its regulator phospholamban are required for cardiovascular function. Phospholamban alters the apparent calcium affinity of SERCA in a process that is modulated by phosphorylation via the β-adrenergic pathway. This regulatory axis allows for the dynamic control of SR calcium stores and cardiac contractility. Herein we focus on hereditary mutants of phospholamban that are associated with heart failure, such as Arg9-Cys, Arg9-Leu, Arg9-His, and Arg14-deletion. Each mutant has a distinct effect on PLN function and SR calcium homeostasis. Arg9-Cys and Arg9-Leu do not inhibit SERCA, Arg14-deletion is a partial inhibitor, and Arg9-His is comparable to wild-type. While the mutants have distinct functional effects on SERCA, they have in common that they cannot be phosphorylated by protein kinase A (PKA). Arg9 and Arg14 are required for PKA recognition and phosphorylation of PLN. Thus, mutations at these positions eliminate β-adrenergic control and dynamic cardiac contractility. Hydrophobic mutations of Arg9 cause more complex changes in function, including loss of PLN function and dominant negative interaction with SERCA in heterozygous individuals. In addition, aberrant interaction with PKA may prevent phosphorylation of wild-type PLN and sequester PKA from other local subcellular targets. Herein we consider what is known about each mutant and how the synergistic changes in SR calcium homeostasis lead to impaired cardiac contractility and dilated cardiomyopathy.
      Citation: Biochemistry and Cell Biology
      PubDate: Mon, 01 Dec 2014 08:00:00 GMT
      DOI: 10.1139/bcb-2014-0080
  • MicroRNA-139-5p regulates C2C12 cell myogenesis through blocking
           Wnt/β-catenin signaling pathway
    • Authors: Lin Mi, Youlei Li, Qiangling Zhang, Chen Zhao, Ying Peng, Gongshe Yang, Xueli Zheng
      Pages: 8 - 15
      Abstract: Biochemistry and Cell Biology, Volume 93, Issue 1, Page 8-15, February 2015. MicroRNAs (miRNAs) are novel and potent regulators in myogenesis. However, the molecular mechanisms that many miRNAs regulate myoblast proliferation and differentiation which are largely unknown. Here, we found that miR-139-5p increased during C2C12 myoblast proliferation, while presenting an inverse trend during C2C12 myoblast differentiation. Flow cytometry and EdU incorporation assay showed that miR-139-5p slowed down the growth of C2C12 cells. Additional study demonstrated that ectopic introduction of miR-139-5p into C2C12 cells blocked myoblast differentiation. Importantly, we demonstrated for the first time that Wnt1, which is associated with the Wnt/β-catenin signaling pathway, was a direct target of miR-139-5p. Moreover, we found that the expression level of Wnt1 was suppressed significantly (p < 0.01) by miR-139-5p, which triggered inhibition of Wnt/β-catenin signaling through upregulation of glycogen synthase kinase 3 beta (GSK-3β; p < 0.05) and downregulation of p-GSK-3β (p < 0.01), β-catenin (p < 0.05), and nuclear β-catenin (p < 0.01). Taken together, these results suggest that miR-139-5p is an important negative regulator in myogenesis through blocking the Wnt1-mediated Wnt/β-catenin signaling pathway.
      Citation: Biochemistry and Cell Biology
      PubDate: Tue, 02 Sep 2014 07:00:00 GMT
      DOI: 10.1139/bcb-2014-0079
  • Inhibitory effects of kaempferol on the invasion of human breast carcinoma
           cells by downregulating the expression and activity of matrix
    • Authors: Chenglin Li, Yuanwei Zhao, Dan Yang, Yanyan Yu, Hao Guo, Ziming Zhao, Bei Zhang, Xiaoxing Yin
      Pages: 16 - 27
      Abstract: Biochemistry and Cell Biology, Volume 93, Issue 1, Page 16-27, February 2015. Matrix metalloproteinases (MMPs) have been regarded as major critical molecules assisting tumor cells during metastasis, for excessive ECM (ECM) degradation, and cancer cell invasion. In the present study, in vitro and in vivo assays were employed to examine the inhibitory effects of kaempferol, a natural polyphenol of flavonoid family, on tumor metastasis. Data showed that kaempferol could inhibit adhesion, migration, and invasion of MDA-MB-231 human breast carcinoma cells. Moreover, kaempferol led to the reduced activity and expression of MMP-2 and MMP-9, which were detected by gelatin zymography, real-time PCR, and western blot analysis, respectively. Further elucidation of the mechanism revealed that kaempferol treatment inhibited the activation of transcription factor activator protein-1 (AP-1) and MAPK signaling pathway. Moreover, kaempferol repressed phorbol-12-myristate-13-acetate (PMA)-induced MMP-9 expression and activity through suppressing the translocation of protein kinase Cδ (PKCδ) and MAPK signaling pathway. Our results also indicated that kaempferol could block the lung metastasis of B16F10 murine melanoma cells as well as the expression of MMP-9 in vivo. Taken together, these results demonstrated that kaempferol could inhibit cancer cell invasion through blocking the PKCδ/MAPK/AP-1 cascade and subsequent MMP-9 expression and its activity. Therefore, kaempferol might act as a therapeutic potential candidate for cancer metastasis.
      Citation: Biochemistry and Cell Biology
      PubDate: Fri, 12 Sep 2014 07:00:00 GMT
      DOI: 10.1139/bcb-2014-0067
  • Multi-physiopathological consequences of the c.1392G>T CFTR mutation
           revealed by clinical and cellular investigations
    • Authors: Raed Farhat, Ayman El-Seedy, Kamal El-Moussaoui, Marie-Claude Pasquet, Catherine Adolphe, Eric Bieth, Jeanne Languepin, Isabelle Sermet-Gaudelus, Alain Kitzis, Véronique Ladevèze
      Pages: 28 - 37
      Abstract: Biochemistry and Cell Biology, Volume 93, Issue 1, Page 28-37, February 2015. This study combines a clinical approach and multiple level cellular analyses to determine the physiopathological consequences of the c.1392G>T (p.Lys464Asn) CFTR exon 10 mutation, detected in a CF patient with a frameshift deletion in trans and a TG(11)T(5) in cis. Minigene experiment, with different TG(m)T(n) alleles, and nasal cell mRNA extracts were used to study the impact of c.1392G>T on splicing in both in cellulo and in vivo studies. The processing and localization of p.Lys464Asn protein were evaluated, in cellulo, by western blotting analyses and confocal microscopy. Clinical and channel exploration tests were performed on the patient to determine the exact CF phenotype profile and the CFTR chloride transport activity. c.1392G>T affects exon 10 splicing by inducing its complete deletion and encoding a frameshift transcript. The polymorphism TG(11)T(5) aggravates the effects of this mutation on aberrant splicing. Analysis of mRNA obtained from parental airway epithelial cells confirmed these in cellulo results. At the protein level the p.Lys464Asn protein showed neither maturated form nor membrane localization. Furthermore, the in vivo channel tests confirmed the absence of CFTR activity. Thus, the c.1392G>T mutation alone or in association with the TG repeats and the poly T tract revealed obvious impacts on splicing and CFTR protein processing and functionality. The c.[T(5); 1392G>T] complex allele contributes to the CF phenotype by affecting splicing and inducing a severe misprocessing defect. These results demonstrate that the classical CFTR mutations classification is not sufficient: in vivo and in cellulo studies of a possible complex allele in a patient are required to provide correct CFTR mutation classification, adequate medical counseling, and adapted therapeutic strategies.
      Citation: Biochemistry and Cell Biology
      PubDate: Wed, 17 Sep 2014 07:00:00 GMT
      DOI: 10.1139/bcb-2014-0042
  • C/EBPβ regulates P2X7 receptor expression in response to glucose
           challenge in intestinal epithelial cells
    • Authors: Maude S. Bilodeau, Guillaume Arguin, Fernand-Pierre Gendron
      Pages: 38 - 46
      Abstract: Biochemistry and Cell Biology, Volume 93, Issue 1, Page 38-46, February 2015. Activation of the ATP-dependent P2X7 receptor modulates glucose transport in intestinal epithelial cells through the downregulation of glucose transporter GLUT2. In the present study, we show that an increase in glucose concentration stimulates P2X7 receptor transcription via modulation of CCAAT/enhancer binding proteins (C/EBPs) α and β expression. The described human P2X7 receptor promoter region (GenBank Y12851) was cloned upstream of a luciferase reporter gene in pGL4.10 plasmid and used to determine whether C/EBPs, namely C/EBPα and C/EBPβ, are able to stimulate the transcription of P2X7 receptor. Results show that C/EBPβ was the main regulator of P2X7 receptor expression in response to a glucose challenge. Chromatin immunoprecipitation (ChIP) assays further revealed that C/EBPβ occupied the –213 to +6 nt P2X7 promoter region. Surprisingly, C/EBPα was also able to bind this region as revealed by ChIP assays, but without inducing receptor transcription. In fact, C/EBPα and the C/EBPβ-LIP isoform blocked the C/EBPβ-dependent regulation of P2X7 receptor transcription. These findings suggest that glucose is not only the major source of energy for cell function but may also act as a signaling molecule to stimulate the expression of regulatory proteins.
      Citation: Biochemistry and Cell Biology
      PubDate: Wed, 17 Sep 2014 07:00:00 GMT
      DOI: 10.1139/bcb-2014-0098
  • Cortical cholinergic dysregulation as a long-term consequence of neonatal
    • Authors: T.R. Anju, C.S. Paulose
      Pages: 47 - 53
      Abstract: Biochemistry and Cell Biology, Volume 93, Issue 1, Page 47-53, February 2015. Neonatal hypoglycemia limits the glucose supply to cells, affecting the function of brain due to its high energy demand. This can cause long-term consequences in brain function, leading to memory and cognitive deficits. The present study evaluated the cholinergic functional regulation in cerebral cortex of one month old rats exposed to neonatal hypoglycemia to understand the long-term effects of early life stress. Receptor binding and gene expression studies were done in the cerebral cortex to analyze the changes in total muscarinicreceptors, muscarinic M1, M2, M3 receptors, and the enzymes involved in acetylcholine metabolism, cholineacetyl transferase and acetylcholine esterase. Neonatal hypoglycemia decreased total muscarinic receptors (p < 0.001) with reduced muscarinic M1, M2, and M3 receptor genes (p < 0.001) in one month old rats. The reduction in acetylcholine metabolism is indicated by the downregulated cholineacetyl transferase, upregulated acetylcholine esterase, and decreased vesicular acetylcholine transporter expression. These alterations in cholinergic function in one month old rat brain indicates the longterm consequences of neonatal hypoglycemia in cortical function, which can contribute to the onset of many disease conditions in later stages of life.
      Citation: Biochemistry and Cell Biology
      PubDate: Thu, 18 Sep 2014 07:00:00 GMT
      DOI: 10.1139/bcb-2014-0035
  • Identification of transcription factors involved in the transcriptional
           regulation of the CXCL12 gene in rat pancreatic insulinoma Rin-5F cell
    • Authors: Jelena Marković, Aleksandra Uskoković, Nevena Grdović, Svetlana Dinić, Mirjana Mihailović, Jelena Arambašić Jovanović, Goran Poznanović, Melita Vidaković
      Pages: 54 - 62
      Abstract: Biochemistry and Cell Biology, Volume 93, Issue 1, Page 54-62, February 2015. Diabetes is characterized by a deficit in the number of functional pancreatic β-cells. Understanding the mechanisms that stimulate neogenesis of β-cells should contribute to improved maintenance of β-cell mass. Chemokine CXCL12 has recently become established as a novel β-cell growth factor, however the mechanisms controlling its expression require clarification. We investigated the proteins involved in the transcriptional regulation of the rat β-cell CXCL12 gene (Cxcl12). Using the electrophoretic mobility shift assay and chromatin immunoprecipitation, we established the in vitro and in vivo binding of C/EBPβ, C/EBPα, STAT3, p53, FOXO3a, and HMG I/Y to the Cxcl12 promoter. Co-immunoprecipitation experiments revealed protein–protein interactions between YY1 and PARP-1, FOXO3a and PARP-1, Sp1 and PARP-1, p53 and PARP-1, C/EBPβ and PARP-1, YY1 and p53, YY1 and FOXO3a, p53 and FOXO3a, Sp1 and FOXO3a, C/EBPβ and FOXO3a, C/EBPα and FOXO3a, Sp1 and STAT3. Our data lay the foundation for research into the interplay of signaling pathways that determine the β-cell Cxcl12 expression profile.
      Citation: Biochemistry and Cell Biology
      PubDate: Mon, 29 Sep 2014 07:00:00 GMT
      DOI: 10.1139/bcb-2014-0104
  • O-GlcNAc protein modification in C2C12 myoblasts exposed to oxidative
           stress indicates parallels with endogenous antioxidant defense
    • Authors: Tina Tinkara Peternelj, Susan A. Marsh, Christudas Morais, David M. Small, Vincent J. Dalbo, Patrick S. Tucker, Jeff S. Coombes
      Pages: 63 - 73
      Abstract: Biochemistry and Cell Biology, Volume 93, Issue 1, Page 63-73, February 2015. A growing body of evidence demonstrates the involvement of protein modification with O-linked β-N-acetylglucosamine (O-GlcNAc) in the stress response and its beneficial effects on cell survival. Here we investigated protein O-GlcNAcylation in skeletal muscle cells exposed to oxidative stress and the crosstalk with endogenous antioxidant system. The study focused on antioxidant enzymes superoxide dismutase 2 (SOD2), catalase (CAT), and glutathione peroxidase 1 (GPX1), and transcriptional regulators proliferator-activated receptor gamma coactivator 1-α (PGC-1α) and forkhead box protein O1 (FOXO1), which play important roles in oxidative stress response and are known to be O-GlcNAc-modified. C2C12 myoblasts were subjected to 24 h incubation with different reagents, including hydrogen peroxide, diethyl maleate, high glucose, and glucosamine, and the inhibitors of O-GlcNAc cycling enzymes. Surprisingly, O-GlcNAc levels were significantly increased only with glucosamine, whilst other treatments showed no effect. Significant changes at the mRNA level were observed with concomitant upregulation of the genes for O-GlcNAc enzymes and stress-related proteins with oxidizing agents and downregulation of these genes with agents promoting O-GlcNAcylation. Our findings suggest a role of O-GlcNAc in the stress response and indicate an inhibitory mechanism controlling O-GlcNAc levels in the muscle cells. This could represent an important homeostatic regulation of the cellular defense system.
      Citation: Biochemistry and Cell Biology
      PubDate: Wed, 08 Oct 2014 07:00:00 GMT
      DOI: 10.1139/bcb-2014-0106
  • Defining the identity of human adipose-derived mesenchymal stem cells
    • Authors: Elisa Montelatici, Barbara Baluce, Enrico Ragni, Cristiana Lavazza, Valentina Parazzi, Riccardo Mazzola, Giovanna Cantarella, Massimiliano Brambilla, Rosaria Giordano, Lorenza Lazzari
      Pages: 74 - 82
      Abstract: Biochemistry and Cell Biology, Volume 93, Issue 1, Page 74-82, February 2015. Adipose-derived mesenchymal stem cells (ADMSCs) are an ideal population for regenerative medical application. Both the isolation procedure and the culturing conditions are crucial steps, since low yield can limit further cell therapies, especially when minimal adipose tissue harvests are available for cell expansion. To date, a standardized procedure encompassing both isolation sites and expansion methods is missing, thus making the choice of the most appropriate conditions for the preparation of ADMSCs controversial, especially in view of the different applications needed. In this study, we compared the effects of three different commercial media (DMEM, aMEM, and EGM2), routinely used for ADMSCs expansion, and two supplements, FBS and human platelet lysate, recently proven to be an effective alternative to prevent xenogeneic antibody transfer and immune alloresponse in the host. Notably, all the conditions resulted in being safe for ADMSCs isolation and expansion with platelet lysate supplementation giving the highest isolation and proliferation rates, together with a commitment for osteogenic lineage. Then, we proved that the high ADMSC hematopoietic supportive potential is performed through a constant and abundant secretion of both GCSF and SCF. In conclusion, this study further expands the knowledge on ADMSCs, defining their identity definition and offers potential options for in vitro protocols for clinical production, especially related to HSC expansion without use of exogenous cytokines or genetic modifications.
      Citation: Biochemistry and Cell Biology
      PubDate: Mon, 20 Oct 2014 07:00:00 GMT
      DOI: 10.1139/bcb-2014-0094
  • Non-genomic effects of spironolactone and eplerenone in cardiomyocytes of
           neonatal Wistar rats: do they evoke cardioprotective pathways'
    • Authors: Milla Marques Hermidorff, Gabriela de Oliveira Faria, Gabriela de Cassia Sousa Amâncio, Leonardo Vinícius Monteiro de Assis, Mauro César Isoldi
      Pages: 83 - 93
      Abstract: Biochemistry and Cell Biology, Volume 93, Issue 1, Page 83-93, February 2015. Mineralocorticoid receptor (MR) antagonists of aldosterone (spironolactone and eplerenone) display beneficial effects in the treatment of cardiopathies; however, many of these responses are independent of this antagonism. The mechanisms of action of these drugs are not well known; few studies have comparatively evaluated whether eplerenone as well as spironolactone display cardioprotective effects independent of the blockade of aldosterone. To study these mechanisms, which lead to cardioprotective responses, and to evaluate comparatively their effects in vitro, we have evaluated the proliferative effect of spironolactone and eplerenone in primary culture of cardiomyocytes and fibroblasts of neonatal Wistar rats in the presence and absence of aldosterone. Spironolactone and eplerenone promoted proliferation of cardiomyocyte even in the absence of aldosterone, suggesting a signaling pathway independent of the antagonism over aldosterone. Spironolactone was able to reduce the proliferation of fibroblasts and to reverse the proliferation promoted by aldosterone, which was also displayed by eplerenone. To elucidate the biochemical pathways evoked by these drugs, we sought to analyze Ca2+, cAMP, and cGMP, and the activity of PKC and ERK1/2. Spironolactone and eplerenone increased the levels of Ca2+, cGMP and activity of ERK 1/2, and reversed the action of aldosterone on the activity of PKC and ERK1/2. Interestingly, only spironolactone increased the levels of cAMP. Our data support the fact that in addition to aldosterone, both spironolactone and eplerenone display rapid responses (non-genomic) such as an increase on cAMP, Ca2+, and cGMP by spironolactone, and Ca2+ and cGMP by eplerenone. We have observed a more consistent cardioprotection promoted by spironolactone; however, these effects have yet to be tested clinically. Therefore, our data show that these drugs do not only act as an antagonist of MR, but could lead to a new pharmacological classification of these drugs.
      Citation: Biochemistry and Cell Biology
      PubDate: Mon, 13 Oct 2014 07:00:00 GMT
      DOI: 10.1139/bcb-2014-0110
  • A cis-acting element in the promoter of human ether à go-go 1
           potassium channel gene mediates repression by calcitriol in human cervical
           cancer cells
    • Authors: V. Cázares-Ordoñez, R.J. González-Duarte, L. Díaz, M. Ishizawa, S. Uno, V. Ortíz, M.L. Ordoñez-Sánchez, M. Makishima, F. Larrea, E. Avila
      Pages: 94 - 101
      Abstract: Biochemistry and Cell Biology, Volume 93, Issue 1, Page 94-101, February 2015. The human ether à go-go 1 potassium channel (hEAG1) is required for cell cycle progression and proliferation of cancer cells. Inhibitors of hEAG1 activity and expression represent potential therapeutic drugs in cancer. Previously, we have shown that hEAG1 expression is downregulated by calcitriol in a variety of cancer cells. Herein, we provided evidence on the regulatory mechanism involved in such repressive effect in cells derived from human cervical cancer. Our results indicate that repression by calcitriol occurs at the transcriptional level and involves a functional negative vitamin D response element (nVDRE) E-box type in the hEAG1 promoter. The described mechanism in this work implies that a protein complex formed by the vitamin D receptor-interacting repressor, the vitamin D receptor, the retinoid X receptor, and the Williams syndrome transcription factor interact with the nVDRE in the hEAG1 promoter in the absence of ligand. Interestingly, all of these transcription factors except the vitamin D receptor-interacting repressor are displaced from hEAG1 promoter in the presence of calcitriol. Our results provide novel mechanistic insights into calcitriol mode of action in repressing hEAG1 gene expression.
      Citation: Biochemistry and Cell Biology
      PubDate: Wed, 22 Oct 2014 07:00:00 GMT
      DOI: 10.1139/bcb-2014-0073
  • Cytochrome P450 expression in mouse brain: specific isoenzymes involved in
           Phase I metabolizing system of porphyrinogenic agents in both microsomes
           and mitochondria
    • Authors: Jimena Lavandera, Silvina Ruspini, Alcira Batlle, Ana María Buzaleh
      Pages: 102 - 107
      Abstract: Biochemistry and Cell Biology, Volume 93, Issue 1, Page 102-107, February 2015. Brain cytochrome P450 (CYP) metabolizes a variety of drugs to produce their pharmacological effects within the brain. We have previously observed that porphyrinogenic agents altered CYP levels in brain. The aim of this work was to further study the involvement of mice brain mitochondrial and microsomal Phase I drug metabolizing system when porphyrinogenic agents, such as Enflurane, Isoflurane, allylisopropylacetamide, veronal, ethanol, and Griseofulvin were administered. To this end, CYP2E1, CYP2B1, and CYP3A4 expression were measured. NADPH cytochrome P450 reductase (CPR) expression was also determined. Western Blots were performed in microsomes and mitochondria of whole brain. Some of the drugs studied altered expression mainly in microsomes. Chronic Isoflurane augmented mitochondrial isoform, although this anaesthetic diminished microsomal expression. Ethanol and topical Griseofulvin affected expression in microsomes but not in mitochondria. CYP2E1 mitochondrial activity was induced by acute Enflurane; while the activity of the microsomal protein was enhanced in alcoholised animals. Ethanol also induced CYP2E1 expression in microsomes, although Isoflurane provoked opposite effects in mitochondria and microsomes. Expression of CPR was also induced. Several reports support an emergent role of CYP enzymes in the pathogenesis of neurological disorders, so CYP response in brain could be one of the multiples factors influencing porphyria acute attacks.
      Citation: Biochemistry and Cell Biology
      PubDate: Wed, 17 Sep 2014 07:00:00 GMT
      DOI: 10.1139/bcb-2014-0088
  • Influence of maternal overnutrition and gestational diabetes on the
           programming of metabolic health outcomes in the offspring: experimental
    • Authors: Troy J. Pereira, Brittany L. Moyce, Stephanie M. Kereliuk, Vernon W. Dolinsky
      Pages: 1 - 14
      Abstract: Biochemistry and Cell Biology, e-First Articles. The incidence of obesity and type 2 diabetes mellitus have risen across the world during the past few decades and has also reached an alarming level among children. In addition, women are currently more likely than ever to enter pregnancy obese. As a result, the incidence of gestational diabetes mellitus is also on the rise. While diet and lifestyle contribute to these trends, population health data show that maternal obesity and diabetes during pregnancy during critical stages of development are major factors that contribute to the development of chronic disease in adolescent and adult offspring. Fetal programming of metabolic function, through physiological and (or) epigenetic mechanisms, may also have an intergenerational effect, and as a result may perpetuate metabolic disorders in the next generation. In this review, we summarize the existing literature that characterizes how maternal obesity and gestational diabetes mellitus contribute to metabolic and cardiovascular disorders in the offspring. In particular, we focus on animal studies that investigate the molecular mechanisms that are programmed by the gestational environment and lead to disease phenotypes in the offspring. We also review interventional studies that prevent disease with a developmental origin in the offspring.
      Citation: Biochemistry and Cell Biology
      PubDate: Fri, 19 Dec 2014 08:00:00 GMT
      DOI: 10.1139/bcb-2014-0141
  • Acetyl-lysine erasers and readers in the control of pulmonary hypertension
           and right ventricular hypertrophy
    • Authors: Matthew S. Stratton, Timothy A. McKinsey
      Pages: 1 - 9
      Abstract: Biochemistry and Cell Biology, e-First Articles. Acetylation of lysine residues within nucleosomal histone tails provides a crucial mechanism for epigenetic control of gene expression. Acetyl groups are coupled to lysine residues by histone acetyltransferases (HATs) and removed by histone deacetylases (HDACs), which are also commonly referred to as “writers” and “erasers”, respectively. In addition to altering the electrostatic properties of histones, lysine acetylation often creates docking sites for bromodomain-containing “reader” proteins. This review focuses on epigenetic control of pulmonary hypertension (PH) and associated right ventricular (RV) cardiac hypertrophy and failure. Effects of small molecule HDAC inhibitors in pre-clinical models of PH are highlighted. Furthermore, we describe the recently discovered role of bromodomain and extraterminal (BET) reader proteins in the control of cardiac hypertrophy, and provide evidence suggesting that one member of this family, BRD4, contributes to the pathogenesis of RV failure. Together, the data suggest intriguing potential for pharmacological epigenetic therapies for the treatment of PH and right-sided heart failure.
      Citation: Biochemistry and Cell Biology
      PubDate: Tue, 16 Dec 2014 08:00:00 GMT
      DOI: 10.1139/bcb-2014-0119
  • Grape seed proanthocyanidins ameliorates cadmium-induced renal injury and
           oxidative stress in experimental rats through the up-regulation of nuclear
           related factor 2 and antioxidant responsive elements
    • Authors: Bashir Nazima, Vaihundam Manoharan, Selvaraj Miltonprabu
      Pages: 1 - 17
      Abstract: Biochemistry and Cell Biology, e-First Articles. Cadmium (Cd) preferentially accumulates in the kidney, the major target for Cd-related toxicity. Cd-induced reactive oxygen species (ROS) have been considered crucial mediators for renal injury. The biologically significant ionic form of cadmium (Cd+) binds to many bio-molecules, and these interactions underlie the toxicity mechanisms of Cd. The present study was hypothesized to explore the protective effect of grape seed proanthocyanidins (GSP) on Cd-induced renal toxicity and to elucidate the potential mechanism. Male Wistar rats were treated with Cd as cadmium chloride (CdCl2, 5 mg·kg−1 bw, orally) and orally pre-administered with GSP (100 mg·kg−1 bw) 90 min before Cd intoxication for 4 weeks to evaluate renal damage of Cd and antioxidant potential of GSP. Serum renal function parameters (blood urea nitrogen and creatinine) levels in serum and urine, renal oxidative stress (lipid peroxidation, protein carbonylation, enzymatic, and non-enzymatic antioxidants), inflammatory (NF-κB p65, NO, TNF-α, IL-6), apoptotic (caspase-3, caspase-9, Bax, Bcl-2), membrane bound ATPases, and Nrf2 (HO-1, keap1, γ-GCS, and μ-GST) markers were evaluated in Cd-treated rats. Pretreatment with GSP revealed a significant improvement in renal oxidative stress markers in kidneys of Cd-treated rats. In addition, GSP treatment decreases the amount of iNOS, NF-κB, TNF-α, caspase-3, and Bax and increases the levels Bcl-2 protein expression. Similarly, mRNA and protein analyses substantiated that GSP treatment notably normalizes the renal expression of Nrf2/Keap1 and its downstream regulatory proteins in the Cd-treated rats. Histopathological and ultra-structural observations also demonstrated that GSP effectively protects the kidney from Cd-induced oxidative damage. These findings suggest that GSP ameliorates renal dysfunction and oxidative stress through the activation of Nrf2 pathway in Cd-intoxicated rats.
      Citation: Biochemistry and Cell Biology
      PubDate: Thu, 11 Dec 2014 08:00:00 GMT
      DOI: 10.1139/bcb-2014-0114
  • Spiraeoside inhibits mast cells activation and IgE-mediated allergic
           responses by suppressing phospholipase C-γ-mediated signaling
    • Authors: Jung Kuk Kim, Young-Kyo Seo, Sehoon Park, Soo-Ah Park, Seyoung Lim, Susie Lee, Ohman Kwon, Jeong Kon Seo, Ung-Kyu Choi, Sung Ho Ryu, Pann-Ghill Suh
      Pages: 1 - 9
      Abstract: Biochemistry and Cell Biology, e-First Articles. Mast cells are responsible for IgE-mediated allergic responses through the secretion of various inflammatory cytokines and mediators. Therefore, the pharmacological regulation of mast cell activation is an important goal in the development of novel anti-allergic drugs. In this study, we found that spiraeoside (SP) inhibits mast cell activation and allergic responses in vivo. SP dose-dependently inhibited the degranulation induced by IgE-antigen (Ag) stimulation in RBL-2H3 mast cells without cytotoxic effects. At the molecular level, SP reduced the Ag-induced phosphorylation and subsequent activation of phospholipase C-γ2 (PLC-γ2). Moreover, SP inhibited the phosphorylation of spleen tyrosine kinase (Syk), linker for activation of T cells (LAT), and downstream MAPKs, such as ERK1/2, p38, and JNK, eventually attenuating expression of TNF-α and IL-4. Finally, we found that SP significantly inhibited IgE-mediated passive cutaneous anaphylaxis (PCA) in mice. Taken together, our results strongly suggest that SP suppresses IgE-mediated mast cell activation and allergic responses by inhibiting Lyn-induced PLC-γ2/MAPK signaling in mast cells.
      Citation: Biochemistry and Cell Biology
      PubDate: Mon, 08 Dec 2014 08:00:00 GMT
      DOI: 10.1139/bcb-2014-0055
  • Cardiovascular complications of type 2 diabetes in youth
    • Authors: D. Scott Kehler, Andrew N. Stammers, Shanel E. Susser, Naomi C. Hamm, Dustin E. Kimber, Michael W. Hlynsky, Todd A. Duhamel
      Pages: 1 - 15
      Abstract: Biochemistry and Cell Biology, e-First Articles. The prevalence of type 2 diabetes mellitus (T2DM) in youth has increased dramatically over the past decades. The literature also suggests that the progression from an impaired glucose tolerance state to established T2DM is more rapid in youth, compared to adults. The presence of significant cardiovascular complications in youth with T2DM, including cardiac, macrovascular, and microvascular remodeling, is another major issue in this younger cohort and poses a significant threat to the healthcare system. However, this issue is only now emerging as a major public health concern, with few data to support optimal treatment targets and strategies to reduce cardiovascular disease (CVD) risk in youth with T2DM. Accordingly, the purpose of this minireview is to better understand the cardiovascular complications in youth with T2DM. We briefly describe the pathophysiology from youth studies, including oxidative stress, inflammation, renin-angiotensin aldosterone system, and epigenetics, which link T2DM and CVD. We also describe the literature concerning the early signs of CVD in youth and potential treatment options to reduce cardiovascular risk.
      Citation: Biochemistry and Cell Biology
      PubDate: Sun, 07 Dec 2014 08:00:00 GMT
      DOI: 10.1139/bcb-2014-0118
  • Purification and photobiochemical profile of photosystem 1 from a
           high-salt tolerant, oleaginous Chlorella (Trebouxiophycaea, Chlorophyta)
    • Authors: Michael D. McConnell, David Lowry, Troy N. Rowan, Karin van Dijk, Kevin E. Redding
      Pages: 1 - 11
      Abstract: Biochemistry and Cell Biology, e-First Articles. The eukaryotic green alga Chlamydomonas reinhardtii has been studied extensively within the biofuel industry as a model organism, as researchers look towards algae to provide chemical feedstocks (i.e., lipids) for the production of liquid transportation fuels. C. reinhardtii, however, is unsuitable for high-level production of such precursors due to its relatively poor lipid accumulation and fresh-water demand. In this study we offer insight into the primary light harvesting and electron transfer reactions that occur during phototropic growth in a high-salt tolerant strain of Chlorella (a novel strain introduced here as NE1401), a single-celled eukaryotic algae also in the phylum Chlorophyta. Under nutrient starvation many eukaryotic algae increase dramatically the amount of lipids stored in lipid bodies within their cell interiors. Microscopy and lipid analyses indicate that Chlorella sp. NE1401 may become a superior candidate for algal biofuels production. We have purified highly active Photosystem 1 (PS1) complexes to study in vitro, so that we may understand further the photobiochemisty of this promising biofuel producer and how its characteristics compare and contrast with that of the better understood C. reinhardtii. Our findings suggest that the PS1 complex from Chlorella sp. NE1401 demonstrates similar characteristics to that of C. reinhardtii with respect to light-harvesting and electron transfer reactions. We also illustrate that the relative extent of the light state transition performed by Chlorella sp. NE1401 is smaller compared to C. reinhardtii, although they are triggered by the same dynamic light stresses.
      Citation: Biochemistry and Cell Biology
      PubDate: Tue, 02 Dec 2014 08:00:00 GMT
      DOI: 10.1139/bcb-2014-0144
  • Berberine as a therapy for type 2 diabetes and its complications: From
           mechanism of action to clinical studies
    • Authors: Wenguang Chang, Li Chen, Grant M. Hatch
      Pages: 1 - 8
      Abstract: Biochemistry and Cell Biology, e-First Articles. The incidence of type 2 diabetes is increasing rapidly worldwide, and the development of novel anti-diabetic drugs is emerging. However, most anti-diabetic drugs cannot be used in patients with hepatic dysfunction, renal disease, and heart disease, which makes pharmacological therapy of type 2 diabetes complicated. Despite continued introduction of novel agents, the search for an ideal drug that is useful as both a hypoglycemic agent and to reduce diabetes-related complications remains elusive. Berberine is an isoquinoline alkaloid extract that has shown promise as a hypoglycemic agent in the management of diabetes in animal and human studies. Mechanistic studies have revealed beneficial effects of berberine on diabetes-related complications. Although there have been few clinical reports of the anti-diabetic effects of berberine, little documentation of adverse effects in humans positions it as a potential candidate drug to treat type 2 diabetes. In the present review, the anti-diabetic mechanism of berberine, its effect on diabetes-related complications, and its recent use in human clinical studies is highlighted. In addition, we summarize the different treatments for type 2 diabetes in adults and children.
      Citation: Biochemistry and Cell Biology
      PubDate: Mon, 01 Dec 2014 08:00:00 GMT
      DOI: 10.1139/bcb-2014-0107
  • Trigonella foenum-graecum ameliorates acrylamide-induced toxicity in rats:
           Roles of oxidative stress, proinflammatory cytokines, and DNA damage
    • Authors: Mohamed M. Abdel-Daim, Mabrouk A. Abd Eldaim, Abeer G.A. Hassan
      Pages: 1 - 7
      Abstract: Biochemistry and Cell Biology, e-First Articles. Acrylamide is a hazardous substance inducing oxidative stress. Based on some evidence on the antioxidant properties of fenugreek, Trigonella foenum-graecum, this study was conducted to investigate the protective effect of fenugreek seed oil against acrylamide toxicity. Thirty-two male Wistar rats were randomly assigned into four groups. The control group was given normal saline. The second group was administered acrylamide (20 mg/kg bw orally). The third and fourth groups were administered acrylamide (20 mg/kg bw) and supplemented with 2.5% and 5% fenugreek seed oil in their diets, respectively. Acrylamide intoxication significantly increased serum levels of LDH, AST, ALT, APL, γ-GT, cholesterol, uric acid, urea, creatinine, 8-oxo-2′-deoxyguanosine, interleukin 1 beta, interleukin 6, and tumor necrosis factor α. Moreover, it increased hepatic, renal, and brain lipid peroxidation, while it impaired the activities and concentrations of the antioxidant biomarkers. Fenugreek oil supplementation normalized the altered serum parameters, prevented lipid peroxidation, and enhanced the antioxidant biomarker concentrations and activities in the hepatic, renal, and brain tissues of acrylamide-intoxicated rats in a dose-dependent manner. Thus, these results indicate that Trigonella foenum-graecum oil has a protective effect against acrylamide-induced toxicity through its free radical scavenging and potent antioxidant activities.
      Citation: Biochemistry and Cell Biology
      PubDate: Mon, 01 Dec 2014 08:00:00 GMT
      DOI: 10.1139/bcb-2014-0122
  • Cardioprotective properties of citicoline against hyperthyroidism-induced
           reperfusion damage in rat hearts
    • Authors: Luz Hernández-Esquivel, Natalia Pavón, Mabel Buelna-Chontal, Héctor González-Pacheco, Javier Belmont, Edmundo Chávez
      Pages: 1 - 7
      Abstract: Biochemistry and Cell Biology, e-First Articles. Hyperthyroidism represents an increased risk factor for cardiovascular morbidity, especially when the heart is subjected to an ischemia/reperfusion process. The aim of this study was to explore the possible protective effect of the nucleotide citicoline on the susceptibility of hyperthyroid rat hearts to undergo reperfusion-induced damage, which is associated with mitochondrial dysfunction. Hence, we analyzed the protective effect of citicoline on the electrical behavior and on the mitochondrial function in rat hearts. Hyperthyroidism was established after a daily i.p. injection of triiodothyronine (at 2 mg/kg of body weight) during 5 days. Thereafter, citicoline was administered i.p. (at 125 mg/kg of body weight) for 5 days. In hyperthyroid rat hearts, citicoline protected against reperfusion-induced ventricular arrhythmias. Moreover, citicoline maintained the accumulation of mitochondrial Ca2+, allowing mitochondria to reach a high transmembrane electric gradient that protected against the release of cytochrome c. It also preserved the activity of the enzyme aconitase that inhibited the release of cytokines. The protection also included the inhibition of oxidative stress-induced mDNA disruption. We conclude that citicoline protects against the reperfusion damage that is found in the hyperthyroid myocardium. This effect might be due to its inhibitory action on the permeability transition in mitochondria.
      Citation: Biochemistry and Cell Biology
      PubDate: Tue, 18 Nov 2014 08:00:00 GMT
      DOI: 10.1139/bcb-2014-0116
  • Associations between visceral fat and liver fat with insulin sensitivity
           and metabolic risk in obese adolescents
    • Authors: Ruth E. Brown, Jennifer L. Kuk, Ingrid Libman, Michelle Rivera-Vega, SoJung Lee
      Pages: 1 - 6
      Abstract: Biochemistry and Cell Biology, e-First Articles. We examined the joint and independent associations between VAT and LF with insulin sensitivity (IS) and lipids in seventy-one obese adolescents (BMI ≥ 95th, 14.9 ± 1.8 years). VAT was assessed by magnetic resonance imaging, and LF was quantified by proton magnetic resonance spectroscopy. IS was evaluated by a 3 -h hyperinsulinemic (80 mU·m−2·min−1) euglycemic clamp. Independent associations between VAT and LF on metabolic variables were assessed in mutually adjusted multivariate models. The joint association between VAT and LF on metabolic variables was assessed by categorizing participants into a low VAT + low LF group (n = 35), high VAT + low LF group (n = 26), or high VAT + high LF group (n = 10), based on a VAT median split (1.17 kg) and high (≥5%) and low (
      Citation: Biochemistry and Cell Biology
      PubDate: Mon, 17 Nov 2014 08:00:00 GMT
      DOI: 10.1139/bcb-2014-0064
  • Isolation of autophagosome subpopulations after induction of autophagy by
    • Authors: Xi Chen, Lin-Jie Li, Xiao-Yu Zheng, Hong-Qiang Shen, Shi-Qiang Shang
      Pages: 1 - 5
      Abstract: Biochemistry and Cell Biology, e-First Articles. Autophagy is a dynamic process accomplished by the generation and maturation of autophagosomes. Isolation of autophagosomes and subsequent compositional analysis can provide information about their biogenesis mechanism. In this article, HEK293 cells expressing GFP-LC3 were treated by calcium phosphate precipitates (CPP) to induce autophagy. The autophaogomes induced by CPP were tubular and vesicular structures, extensively formed in the cytosol. After all membranes in the cell lysate were fractionated by differential centrifugation, autophagosomes from light and heavy membranes were isolated by immuno-precipitation, using antibodies against GFP-LC3 and Atg5. We found that GFP-LC3 and Atg5 positive autophagosomes represented distinctive subpopulations. Judged from the molecular markers associated, including organelle markers and Atg proteins, GFP-LC3 positive autophagosomes were overall at the later biogenetic stage. Furthermore, both GFP-LC3 and Atg5 positive autophagosomes from light membranes were less mature than those from heavy membranes. We have established a method to isolate subpopulations of autophagsomes for further characterization.
      Citation: Biochemistry and Cell Biology
      PubDate: Thu, 13 Nov 2014 22:33:37 GMT
      DOI: 10.1139/bcb-2014-0115
  • New insights into lung development and diseases: the role of microRNAs
    • Authors: Dina Johar, Vinayakumar Siragam, Thomas H. Mahood, Richard Keijzer
      Pages: 1 - 10
      Abstract: Biochemistry and Cell Biology, e-First Articles. MicroRNAs (miRNAs) are short endogenous noncoding RNA molecules (∼22 nucleotides) that can regulate gene expression at the post-transcription level. Research interest in the role of miRNAs in lung biology is emerging. MiRNAs have been implicated in a range of processes such as development, homeostasis, and inflammatory diseases in lung tissues and are capable of inducing differentiation, morphogenesis, and apoptosis. In recent years, several studies have reported that miRNAs are differentially regulated in lung development and lung diseases in response to epigenetic changes, providing new insights for their versatile role in various physiological and pathological processes in the lung. In this review, we discuss the contribution of miRNAs to lung development and diseases and possible future implications in the field of lung biology.
      Citation: Biochemistry and Cell Biology
      PubDate: Fri, 07 Nov 2014 22:35:08 GMT
      DOI: 10.1139/bcb-2014-0103
  • Epigenetic contributions to the developmental origins of adult lung
    • Authors: Lisa A. Joss-Moore, Robert H. Lane, Kurt H. Albertine
      Pages: 1 - 9
      Abstract: Biochemistry and Cell Biology, e-First Articles. Perinatal insults, including intrauterine growth restriction, preterm birth, maternal exposure to toxins, or dietary deficiencies produce deviations in the epigenome of lung cells. Occurrence of perinatal insults often coincides with the final stages of lung development. The result of epigenome disruptions in response to perinatal insults during lung development may be long-term structural and functional impairment of the lung and development of lung disease. Understanding the contribution of epigenetic mechanisms to life-long lung disease following perinatal insults is the focus of the developmental origins of adult lung disease field. DNA methylation, histone modifications, and microRNA changes are all observed in various forms of lung disease. However, the perinatal contribution to such epigenetic mechanisms is poorly understood. Here we discuss the developmental origins of adult lung disease, the interplay between perinatal events, lung development and disease, and the role that epigenetic mechanisms play in connecting these events.
      Citation: Biochemistry and Cell Biology
      PubDate: Mon, 13 Oct 2014 21:33:28 GMT
      DOI: 10.1139/bcb-2014-0093
  • The role of miR-29 in pulmonary fibrosis
    • Authors: Leah Cushing, Pingping Kuang, Jining Lü
      Pages: 1 - 10
      Abstract: Biochemistry and Cell Biology, e-First Articles. Pulmonary fibrosis is a pathological condition in which lungs become scarred due to the excess extracellular matrix (ECM) deposition and structural alterations in the interstitium of lung parenchyma. Many patients with interstitial lung diseases (ILDs) caused by long-term exposure to toxic substances, chronic infections, or autoimmune responses develop fibrosis. Etiologies for many ILDs are unknown, such as idiopathic pulmonary fibrosis (IPF), a devastating, relentless form of pulmonary fibrosis with a median survival of 2–3 years. Despite several decades of research, factors that initiate and sustain the fibrotic response in lungs remain unclear and there is no effective treatment to block progression of fibrosis. Here we summarize recent findings on the antifibrotic activity of miR-29, a small noncoding regulatory RNA, in the pathogenesis of fibrosis by regulating ECM production and deposition, and epithelial–mesenchymal transition (EMT). We also describe interactions of miR-29 with multiple profibrotic and inflammatory pathways. Finally, we review the antifibrotic activity of miR-29 in animal models of fibrosis and highlight miR-29 as a promising therapeutic reagent or target for the treatment of pulmonary fibrosis.
      Citation: Biochemistry and Cell Biology
      PubDate: Thu, 18 Sep 2014 21:36:33 GMT
      DOI: 10.1139/bcb-2014-0095
  • PANC-1 cells proliferative response to ionizing radiation is related to
           GSK-3β phosphorylation
    • Authors: Nora A. Mohamad, Graciela P. Cricco, Claudia M. Cocca, Elena S. Rivera, Rosa M. Bergoc, Gabriela A. Martín
      Pages: 1 - 12
      Abstract: Biochemistry and Cell Biology, e-First Articles. Radiotherapy may be used to treat pancreatic cancer and relieve pain. We have previously reported that histamine modulates pancreatic adenocarcinoma PANC-1 cell proliferation. This work was aimed to evaluate whether histamine improves radiosensitivity of PANC-1 cells in relation to phosphorylation/inhibition of glycogen synthase kinase-3β (GSK-3β). Immediately after γ irradiation, intracellular hydrogen peroxide was markedly decreased together with a rapid increase in catalase activity. Although histamine diminished catalase activity in nonirradiated cells, it only partially hindered the increase observed in irradiated cells and could not modify radiosensitivity. In control cells, a high expression of total and a very low expression of phosphorylated/inactive GSK-3β were found. An increment in reactive oxygen species levels produced an augmentation in GSK-3β phosphorylation and suppressed cell proliferation. In both control and histamine-treated irradiated cells, the rise in catalase activity lowered reactive oxygen species levels and only a small increase in phosphorylated GSK-3β was detected. Alternatively, 3-aminotriazole, an irreversible inhibitor of catalase, reduced the survival fraction in irradiated control cells along with an increment in phosphorylated GSK-3β. These results suggest that upon irradiation, early catalase activation may be responsible for keeping GSK-3β active conceding cells a survival advantage toward cytotoxic effects of ionizing radiation.
      Citation: Biochemistry and Cell Biology
      PubDate: Sun, 25 Nov 2012 15:55:27 GMT
      DOI: 10.1139/bcb-2012-032
  • Utp22p acts in concert with Utp8p to channel aminoacyl-tRNA from the
           nucleolus to the nuclear tRNA export receptor Los1p but not Msn5p
    • Authors: Manoja B.K. Eswara, Ashley Clayton, Dev Mangroo
      Pages: 1 - 19
      Abstract: Biochemistry and Cell Biology, e-First Articles. Utp8p is an essential nucleolar protein that channels aminoacyl-tRNAs from aminoacyl-tRNA synthetases in the nucleolus to the nuclear tRNA export receptors located in the nucleoplasm and nuclear pore complex in Saccharomyces cerevisiae. Utp8p is also part of the U3 snoRNA-associated protein complex involved in 18S rRNA biogenesis in the nucleolus. We report that Utp22p, which is another member of the U3 snoRNA-associated protein complex, is also an intranuclear component of the nuclear tRNA export machinery. Depletion of Utp22p results in nuclear retention of mature tRNAs derived from intron-containing and intronless precursors. Moreover, Utp22p copurifies with the nuclear tRNA export receptor Los1p, the aminoacyl-tRNA synthetase Tys1p and Utp8p, but not with the RanGTPase Gsp1p and the nuclear tRNA export receptor Msn5p. Utp22p interacts directly with Utp8p and Los1p in a tRNA-independent manner in vitro. Utp22p also interacts directly with Tys1p, but this binding is stimulated when Tys1p is bound to tRNA. However, Utp22p, unlike Utp8p, does not bind tRNA saturably. These data suggest that Utp22p recruits Utp8p to aminoacyl-tRNA synthetases in the nucleolus to collect aminoacyl-tRNA and then accompanies the Utp8p–tRNA complex to deliver the aminoacyl-tRNAs to Los1p but not Msn5p. It is possible that Nrap/Nol6, the mammalian orthologue of Utp22p, plays a role in channelling aminoacyl-tRNA to the nuclear tRNA export receptor exportin-t.
      Citation: Biochemistry and Cell Biology
      PubDate: Tue, 20 Nov 2012 13:45:45 GMT
      DOI: 10.1139/bcb-2012-034
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