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BIOLOGY (1422 journals)

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Journal Cover Biochemistry and Cell Biology
  [SJR: 0.859]   [H-I: 76]   [14 followers]  Follow
   Hybrid Journal Hybrid journal (It can contain Open Access articles)
   ISSN (Print) 0829-8211 - ISSN (Online) 1208-6002
   Published by NRC Research Press Homepage  [21 journals]
  • Modulation of amyloid assembly by glycosaminoglycans: from mechanism to
           biological significance
    • Pages: 329 - 337
      Abstract: Biochemistry and Cell Biology, Volume 95, Issue 3, Page 329-337, June 2017.
      Glycosaminoglycans (GAGs) are long and unbranched polysaccharides that are abundant in the extracellular matrix and basement membrane of multicellular organisms. These linear polyanionic macromolecules are involved in many physiological functions from cell adhesion to cellular signaling. Interestingly, amyloid fibrils extracted from patients afflicted with protein misfolding diseases are virtually always associated with GAGs. Amyloid fibrils are highly organized nanostructures that have been historically associated with pathological states, such as Alzheimer’s disease and systemic amyloidoses. However, recent studies have identified functional amyloids that accomplish crucial physiological roles in almost all living organisms, from bacteria to insects and mammals. Over the last 2 decades, numerous reports have revealed that sulfated GAGs accelerate and (or) promote the self-assembly of a large diversity of proteins, both inherently amyloidogenic and non-aggregation prone. Despite the fact that many studies have investigated the molecular mechanism(s) by which GAGs induce amyloid assembly, the mechanistic elucidation of GAG-mediated amyloidogenesis still remains the subject of active research. In this review, we expose the contribution of GAGs in amyloid assembly, and we discuss the pathophysiological and functional significance of GAG-mediated fibrillization. Finally, we propose mechanistic models of the unique and potent ability of sulfated GAGs to hasten amyloid fibril formation.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-02-01T08:00:00Z
      DOI: 10.1139/bcb-2016-0236
  • Structural evaluations of tau protein conformation: methodologies and
    • Pages: 338 - 349
      Abstract: Biochemistry and Cell Biology, Volume 95, Issue 3, Page 338-349, June 2017.
      Protein-misfolding diseases are based on a common principle of aggregation initiated by intra- and inter-molecular contacts. The structural and conformational changes induced by biochemical transformations such as post-translational modifications (PTMs), often lead to protein unfolding and misfolding. Thus, these order-to-disorder or disorder-to-order transitions may regulate cellular function. Tau, a neuronal protein, regulates microtubule (MT) structure and overall cellular integrity. However, misfolded tau modified by PTMs results in MT destabilization, toxic tau aggregate formation, and ultimately cell death, leading to neurodegeneration. Currently, the lack of structural information surrounding tau severely limits understanding of neurodegeneration. This minireview focuses on the current methodologies and approaches aimed at probing tau conformation and the role of conformation in various aspects of tau biochemistry. The recent applications of nuclear magnetic resonance, mass spectrometry, Förster resonance electron transfer, and molecular dynamics simulations toward structural analysis of conformational landscapes of tau will be described. The strategies developed for structural evaluation of tau may significantly improve our understanding of misfolding diseases.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-03-09T08:00:00Z
      DOI: 10.1139/bcb-2016-0227
  • Interactions of U24 from Roseolovirus with WW domains: canonical vs
    • Pages: 350 - 358
      Abstract: Biochemistry and Cell Biology, Volume 95, Issue 3, Page 350-358, June 2017.
      U24 is a C-terminal membrane-anchored protein found in both human herpes virus type 6 and 7 (HHV-6 and HHV-7), with an N-terminal segment that is rich in prolines (PPxY motif in both HHV-6A and 7; PxxP motif in HHV-6A). Previous work has shown that U24 interacts strongly with Nedd4 WW domains, in particular, hNedd4L-WW3*. It was also shown that this interaction depends strongly on the nature of the amino acids that are upstream from the PY motif in U24. In this contribution, data was obtained from pull-downs, isothermal titration calorimetry, and NMR to further determine what modulates U24:WW domain interactions. Specifically, 3 non-canonical WW domains from human Smad ubiquitination regulatory factor (Smurf), namely hSmurf2-WW2, hSmurf2-WW3, and a tandem construct hSmurf2-WW2 + 3, were studied. Overall, the interactions between U24 and these Smurf WW domains were found to be weaker than those in U24:Nedd4 WW domain pairs, suggesting that U24 function is tightly linked to specific E3 ubiqitin ligases.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-03-17T07:00:00Z
      DOI: 10.1139/bcb-2016-0250
  • Use of substitute Nonidet P-40 nonionic detergents in intracellular
           tubulin polymerization assays for screening of microtubule targeting
    • Pages: 379 - 384
      Abstract: Biochemistry and Cell Biology, Volume 95, Issue 3, Page 379-384, June 2017.
      Shell Chemical Company Nonidet P-40 has been used for decades in many biochemical assays as a nonionic, nondenaturing detergent; however, Shell no longer manufactures this product. Four commercially available substitutes were investigated and their activities titrated in an intracellular tubulin polymerization assay. Although claimed by the supply companies to be identical to the Shell Nonidet P-40, all four substitutes were about 10-fold more potent and needed to be diluted accordingly. As microtubule targeting drugs are a major class of anticancer agent, and many researchers use the intracellular tubulin polymerization assay, this information is important to help troubleshoot assay development with the new substitutes. As the Shell Nonidet P-40 has been used in many biochemical buffers, these results will be of general interest to the biochemical, cell, and molecular research community.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-01-10T08:00:00Z
      DOI: 10.1139/bcb-2016-0141
  • Lactoferrin interacts with SPLUNC1 to attenuate lipopolysaccharide-induced
           inflammation of human nasal epithelial cells via down-regulated
           MEK1/2-MAPK signaling
    • Pages: 394 - 399
      Abstract: Biochemistry and Cell Biology, Volume 95, Issue 3, Page 394-399, June 2017.
      The short palate, lung, and nasal epithelium clone 1 (SPLUNC1) protein is an important innate material in the upper airway, and lactoferrin (LF) aids the innate functions in humans. In this study, a nasal epithelial model was used to investigate how LF modulates SPLUNC1 to reduce the inflammatory process mediated by lipopolysaccharide (LPS). The inflammation of human RPMI-2650 cells was induced with LPS to evaluate SPLUNC1 expression after treating the cells with bovine LF (bLF). The interaction pathway between LF and SPLUNC1 in LPS-induced inflammation was further investigated. Our study reveals that the addition of bLF results in the recovery of SPLUNC1 expression in nasal epithelial cells under LPS-induced inflammation. MAPK is involved in the main pathway for the SPLUNC1 and bLF interaction. Decreased SPLUNC1 function could be recovered by addition of bLF. The MEK1/2–MAPK signaling pathway is crucial for the SPLUNC1 and bLF interaction. Therefore, LF could support SPLUNC1 in the innate immunity recovery process.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-02-08T08:00:00Z
      DOI: 10.1139/bcb-2016-0047
  • Differential effect of hypoxia and acidity on lung cancer cell and
           fibroblast metabolism
    • Pages: 428 - 436
      Abstract: Biochemistry and Cell Biology, Volume 95, Issue 3, Page 428-436, June 2017.
      This study examined the metabolic response of lung cancer cells and normal lung fibroblasts to hypoxia and acidity. GLUT1 and HXKII mRNA/protein expression was up-regulated under hypoxia in the MRC5 fibroblasts and in the A549 and H1299 lung cancer cell lines, indicating intensified glucose absorption and glycolysis. Under hypoxia, the LDHA mRNA and LDH5 protein levels increased in the cancer cells but not in the fibroblasts. Acidity suppressed the above-mentioned hypoxia effect. PDH-kinase-1 (PDK1 mRNA and protein) and inactive phosphorylated-PDH protein levels were induced under hypoxia in the cancer cells, whereas these were reduced in the MRC5 lung fibroblasts. In human tissue sections, the prevalent expression patterns supported the contrasting metabolic behavior of cancer cells vs. tumor fibroblasts. The monocarboxylate/lactate transporter 1 (MCT1) was up-regulated in all the cell lines under hypoxic conditions, but it was suppressed under acidic conditions. The mitochondrial DNA (mtDNA) content per cell decreased significantly in the A549 cancer cell line under hypoxia, but it increased in the MRC5 fibroblasts. Taking into account these findings, we suggest that, under hypoxia, cancer cells intensify the anaerobic direction in glycolysis, while normal fibroblasts prefer to seek energy by intensifying the aerobic use of the available oxygen.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-01-24T08:00:00Z
      DOI: 10.1139/bcb-2016-0197
  • MicroRNA-181 inhibits proliferation and promotes apoptosis of chondrocytes
           in osteoarthritis by targeting PTEN
    • Pages: 437 - 444
      Abstract: Biochemistry and Cell Biology, Volume 95, Issue 3, Page 437-444, June 2017.
      Objective: To investigate the effects of microRNA-181 (miR-181) on the proliferation and apoptosis of chondrocytes in osteoarthritis (OA) by targeting PTEN. Methods: The chondrocytes in logarithmic growth phase were selected and divided into 6 test groups: the normal, blank, negative control, miR-181 mimic, miR-181 inhibitor, and miR-181 inhibitor + PTEN-siRNA groups. Reverse transcription qPCR was used to detect the expressions of miR-181 and PTEN mRNA. MTT assay and flow cytometry were performed to detect cell proliferation and apoptosis. The protein expressions of PARP and caspase-3 and the activity of MMP-2 and MMP-9 were detected by Western blotting and gelatin zymography assay. Results: The miR-181 mimic group showed increased miR-181 expression and decreased PTEN expression compared with the other 5 groups. Also, by comparison with the other 5 groups, the cell proliferation rate declined and the rate of cell apoptosis was elevated in the miR-181 mimic group. The MiR-181 mimic group showed remarkably increased protein expression of caspase-3 and PARP compared with the other 5 groups. The activity of MMP-2 and MMP-9 was higher in the miR-181 mimic group than the other 5 groups. Conclusion: MiR-181 could up-regulate the expressions of caspase-3, PARP, MMP-2, and MMP-9, and thereby inhibit cell proliferation and promote apoptosis of chondrocytes in OA by targeting PTEN.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-01-25T08:00:00Z
      DOI: 10.1139/bcb-2016-0078
  • Ceruloplasmin-derived peptide is the strongest regulator of oxidative
           stress and leukotriene synthesis in neutrophils
    • Pages: 445 - 449
      Abstract: Biochemistry and Cell Biology, Volume 95, Issue 3, Page 445-449, June 2017.
      Ceruloplasmin, an acute-phase protein, can affect the activity of leukocytes through its various enzymatic activities and protein–protein interactions (with lactoferrin, myeloperoxidase, eosinophil peroxidase, serprocidins, and 5-lipoxygenase (5-LOX), among others). However, the molecular mechanisms of ceruloplasmin activity are not clearly understood. In this study, we tested the ability of two synthetic peptides, RPYLKVFNPR (883–892) (P1) and RRPYLKVFNPRR (882–893) (P2), corresponding to the indicated fragments of the ceruloplasmin sequence, to affect neutrophil activation. Leukotriene (LT) B4 is the primary eicosanoid product of polymorphonuclear leukocytes (PMNLs, neutrophils). We studied leukotriene synthesis in PMNLs upon interaction with Salmonella enterica serovar Typhimurium. Priming of neutrophils with phorbol 12-myristate 13-acetate (PMA) elicited the strong regulatory function of P2 peptide as a superoxide formation inducer and leukotriene synthesis inhibitor. Ceruloplasmin-derived P2 peptide appeared to be a strong inhibitor of 5-LOX product synthesis under conditions of oxidative stress.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-01-10T08:00:00Z
      DOI: 10.1139/bcb-2016-0180
  • Method comparison for analyzing wound healing rates
    • Pages: 450 - 454
      Abstract: Biochemistry and Cell Biology, Volume 95, Issue 3, Page 450-454, June 2017.
      Wound healing scratch assay is a frequently used method to characterize cell migration, which is an important biological process in the course of development, tissue repair, and immune response for example. The measurement of wound healing rate, however, varies among different studies. Here we summarized these measurements into three types: (I) direct rate average; (II) regression rate average; and (III) average distance regression rate. Using Chinese hamster ovary (CHO) cells as a model, we compared the three types of analyses on quantifying the wound closing rate, and discovered that type I & III measurements are more resistant to outliers, and type II analysis is more sensitive to outliers. We hope this study can help researchers to better use this simple yet effective assay.
      Citation: Biochemistry and Cell Biology
      PubDate: 2017-01-30T08:00:00Z
      DOI: 10.1139/bcb-2016-0163
  • Potential regulatory mechanisms of lncRNA in diabetes and its
    • Pages: 361 - 367
      Abstract: Biochemistry and Cell Biology, Volume 95, Issue 3, Page 361-367, June 2017.
      Long non-coding RNAs (lncRNAs) are transcripts longer than 200 nucleotides without protein-coding potential. Although these molecules were initially considered as “junk products” of transcription without biological relevance, recent advances in research have shown that lncRNA plays an important role, not only in cellular processes such as proliferation, differentiation, and metabolism, but also in the pathological processes of cancers, diabetes, and neurodegenerative diseases. In this review, we focus on the potential regulatory roles of lncRNA in diabetes and the complications associated with diabetes.
      Citation: Biochemistry and Cell Biology
      PubDate: 2016-11-21T08:00:00Z
      DOI: 10.1139/bcb-2016-0110
  • Functional assessment of MeCP2 in Rett syndrome and cancers of breast,
           colon, and prostate
    • Pages: 368 - 378
      Abstract: Biochemistry and Cell Biology, Volume 95, Issue 3, Page 368-378, June 2017.
      Ever since the first report that mutations in methyl-CpG-binding protein 2 (MeCP2) causes Rett syndrome (RTT), a severe neurological disorder in females world-wide, there has been a keen interest to gain a comprehensive understanding of this protein. While the classical model associated with MeCP2 function suggests its role in gene suppression via recruitment of co-repressor complexes and histone deacetylases to methylated CpG-sites, recent discoveries have brought to light its role in transcription activation, modulation of RNA splicing, and chromatin compaction. Various post-translational modifications (PTMs) of MeCP2 further increase its functional versatility. Involvement of MeCP2 in pathologies other than RTT, such as tumorigenesis however, remains poorly explored and understood. This review provides a survey of the literature implicating MeCP2 in breast, colon and prostate cancer.
      Citation: Biochemistry and Cell Biology
      PubDate: 2016-11-10T08:00:00Z
      DOI: 10.1139/bcb-2016-0154
  • PRPS1 silencing reverses cisplatin resistance in human breast cancer cells
    • Pages: 385 - 393
      Abstract: Biochemistry and Cell Biology, Volume 95, Issue 3, Page 385-393, June 2017.
      PRPS1 (phosphoribosyl pyrophosphate synthetase 1), which drives the nucleotide biosynthesis pathway, modulates a variety of functions by providing central building blocks and cofactors for cell homeostasis. As tumor cells often display abnormal nucleotide metabolism, dysregulated de-novo nucleotide synthesis has potential impacts in cancers. We now report that PRPS1 is specifically and highly expressed in chemoresistant (CR) cancer cells derived from cisplatin-resistant human breast cancer cell lines SK-BR-3 and MCF-7. The inhibition of PRPS1 activity in CR cells by genetic silencing reduces cell viability and increases apoptosis in vitro, both of which can be further potentiated by cisplatin treatment. Significantly, such down-regulation of PRPS1 in CR cells when administered to nude mice enhanced the survival of those animals, as demonstrated by decreased tumor growth. Knockdown of PRPSI may cause these effects by potently inducing autonomous activation of caspase-3 and inhibiting the proliferation in the engrafted CR tumors. As a result, cisplatin sensitivity in a xenograft model of CR cancer cells can be restored by the down-regulation of PRPS1. Thus, PRPS1 inhibition may afford a therapeutic approach to relapsed patients with breast cancer, resistant to chemotherapy.
      Citation: Biochemistry and Cell Biology
      PubDate: 2016-11-03T07:00:00Z
      DOI: 10.1139/bcb-2016-0106
  • Diosmin attenuates radiation-induced hepatic fibrosis by boosting PPAR-γ
           expression and hampering miR-17-5p-activated canonical Wnt–β-catenin
    • Pages: 400 - 414
      Abstract: Biochemistry and Cell Biology, Volume 95, Issue 3, Page 400-414, June 2017.
      Background: Liver fibrosis is one of the major complications from upper right quadrant radiotherapy. MicroRNA-17-5p (miR-17-5p) is hypothesized to act as a regulator of hepatic stellate cell (HSCs) activation by activation of the canonical Wnt–β-catenin pathway. Diosmin (Dios), a citrus bioflavonoid, is known to possess potent antioxidant, anti-inflammatory, and anti-apoptotic properties. Purpose: To explore the molecular mechanisms that underlie radiation-induced liver fibrosis, and to evaluate the possible influence of Dios on the miR-17-5p–Wnt–β-catenin signaling axis during fibrogenesis provoked by irradiation (IRR) in rats. Also, the effect of Dios on hepatic peroxisome proliferator activated receptor-γ (PPAR-γ) expression as a regulator for HSC activation was considered. Methods: We administered 100 mg·(kg body mass)–1·day–1 (per oral) of Dios were administered to IRR-exposed rats (overall dose of 12 Gy on 6 fractions of 2 Gy each) for 6 successive weeks. Results: Data analysis revealed that Dios treatment mitigated oxidative stress, enhanced antioxidant defenses, alleviated hepatic inflammatory responses, abrogated pro-fibrogenic cytokines, and stimulated PPAR-γ expression. Dios treatment repressed the miR-17-5p activated Wnt–β-catenin signaling induced by IRR. Moreover, Dios treatment restored the normal hepatic architecture and reversed pathological alterations induced by IRR. Conclusion: We hypothesize that the stimulation of PPAR-γ expression and interference with miR-17-5p activated Wnt–β-catenin signaling mediates the antifibrotic properties of Dios.
      Citation: Biochemistry and Cell Biology
      PubDate: 2016-11-21T08:00:00Z
      DOI: 10.1139/bcb-2016-0142
  • Chronic intermittent hypoxia disturbs insulin secretion and causes
           pancreatic injury via the MAPK signaling pathway
    • Pages: 415 - 420
      Abstract: Biochemistry and Cell Biology, Volume 95, Issue 3, Page 415-420, June 2017.
      Obstructive sleep apnea (OSA) is a breathing disorder during sleep, with a most prominent character of chronic intermittent hypoxia (CIH), which induces the generation of reactive oxygen species (ROS) that damages multiple tissues and causes metabolic disorders. In this study, we established a rat model of varying OSA with different grades of CIH (12.5% O2, 10% O2, 7.5% O2, and 5% O2) for 12 weeks, and found that CIH stimulated insulin secretion, reduced the insulin:proinsulin ratio in pancreatic tissue, and caused pancreatic tissue lesions and cell apoptosis in a dose-dependent manner. Moreover, CIH promoted the production of tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6, and activated mitogen-activated protein kinase (MAPK) family members, extracellular regulated protein kinase (ERK), c-Jun N-terminal kinase (JNK), and P38, depending on the O2 concentration. In summary, CIH disturbed insulin secretion, and caused inflammation, lesions, and cell apoptosis in pancreatic tissue via the MAPK signaling pathway, which may be of great significance for clinical treatment of OSA and type 2 diabetes mellitus (T2DM).
      Citation: Biochemistry and Cell Biology
      PubDate: 2016-11-28T08:00:00Z
      DOI: 10.1139/bcb-2016-0167
  • Temporo-spacial microanatomical distribution of the murine
           sodium-dependent ascorbic acid transporters Slc23a1 and Slc23a2 in the
           kidney throughout development
    • Pages: 421 - 427
      Abstract: Biochemistry and Cell Biology, Volume 95, Issue 3, Page 421-427, June 2017.
      The two membrane transporters Slc23a1 and Slc23a2 mediate ascorbic acid uptake into cells. We recently determined the key role of Slc23a1 in renal re-absorption of ascorbic acid in a knockout mouse model. However, the renal spatial and temporal expression patterns of murine Slc23a1 and Slc23a2 are not defined. This study utilizes database evidence combined with experimental confirmation via in-situ hybridization to define the spatial and temporal expression of Slc23a1 in the murine kidney. Slc23a1 is expressed in the early proximal tubule, but not in its precursors during embryonic development, and exclusive proximal tubular expression persists throughout the animal’s lifetime. In contrast, Slc23a2 is uniformly expressed in metabolic cell types such as stromal cells. The expression patterns appear to be conserved from rodent lineages to humans.
      Citation: Biochemistry and Cell Biology
      PubDate: 2016-12-20T08:00:00Z
      DOI: 10.1139/bcb-2015-0090
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