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Source: The International Journal of Biochemistry and Cell Biology

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Total 120 results found since Jan 2013.

Inhibition of KCa3.1 suppresses TGF-β1 induced MCP-1 expression in human proximal tubular cells through Smad3, p38 and ERK1/2 signaling pathways.
In this study, human proximal tubular cells (HK2 cells) were incubated with TGF-β1 (2ng/ml) for 48h in the presence or absence of KCa3.1 siRNA or the KCa3.1 inhibitor TRAM34. HK2 cells overexpressing KCa3.1 were studied in parallel. The mRNA and protein expression of monocyte chemoattractant protein-1 (MCP-1) were measured by qRT-PCR and ELISA. Downstream TGF-β1 signaling molecules Smad3, p38 and ERK1/2 were measured by Western blot analysis. Using whole-cell patch clamp techniques we found that TGFβ-1 induced a large KCa3.1 K(+)-current that was inhibited by TRAM34. TGF-β1 also increased MCP-1 mRNA and protein express...
Source: The International Journal of Biochemistry and Cell Biology - November 28, 2013 Category: Biochemistry Authors: Huang C, Day ML, Poronnik P, Pollock CA, Chen XM Tags: Int J Biochem Cell Biol Source Type: research

Death Receptor 3 Mediates TNFSF15- and TNFα-Induced Endothelial Cell Apoptosis.
Abstract Tumor necrosis factor superfamily 15 (TNFSF15) suppresses angiogenesis by specifically inducing apoptosis in proliferating endothelial cells. Death receptor 3 (DR3), a member of the TNF receptor superfamily (TNFRSF25), has been identified as a receptor for TNFSF15 to activate T cells. It is unclear, however, whether DR3 mediates TNFSF15 activity on endothelial cells. Here we show that siRNA-mediated knockdown of DR3 in an in vivo Matrigel angiogenesis assay, or in adult bovine aortic endothelial (ABAE) cell cultures, leads to resistance of endothelial cells to TNFSF15-induced apoptosis. Interestingly, DR3...
Source: The International Journal of Biochemistry and Cell Biology - August 23, 2014 Category: Biochemistry Authors: Xu LX, Grimaldo S, Qi JW, Yang GL, Qin TT, Xiao HY, Xiang R, Xiao Z, Li LY, Zhang ZS Tags: Int J Biochem Cell Biol Source Type: research

Notch1 Inhibition Reduces Low Shear Stress-Induced Plaque Formation.
Abstract Low shear stress (LSS) contributes to the pathogenesis of inflammatory diseases, such as atherosclerosis. Notch1 is a type I transmembrane receptor that critically determines the growth, differentiation, and survival of various cell types, but its role and mechanism in LSS-induced inflammatory response remains undetermined. Apolipoprotein E-deficient (ApoE(-/-)) mice were fed with high fat diet and administered intraperitoneally with DAPT (a γ-secretase inhibitor). Perivascular shear stress modifiers were placed around the right carotid arteries to induce LSS. The left carotid arteries with undisturbed s...
Source: The International Journal of Biochemistry and Cell Biology - January 16, 2016 Category: Biochemistry Authors: Qin WD, Zhang F, Qin XJ, Wang J, Meng X, Wang H, Guo HP, Wu QZ, Wu DW, Zhang MX Tags: Int J Biochem Cell Biol Source Type: research

The AQP-3 water channel is a pivotal modulator of glycerol-induced chloride channel activation in nasopharyngeal carcinoma cells.
In conclusion, AQP-3 is the pathway for water, glycerol and other small solutes to enter cells, and it may be an essential modulator for the gating of chloride channels. PMID: 26794461 [PubMed - as supplied by publisher]
Source: The International Journal of Biochemistry and Cell Biology - January 18, 2016 Category: Biochemistry Authors: Zhang H, Deng Z, Yang L, Luo H, Liu S, Li Y, Wei Y, Peng S, Zhu L, Wang L, Chen L Tags: Int J Biochem Cell Biol Source Type: research

Hypoxia Decrease Expression of Cartilage Oligomeric Matrix Protein to Promote Phenotype Switching of Pulmonary Arterial Smooth Muscle Cells.
Abstract Extracellular matrix proteins play important roles in the development of pulmonary hypertension(PH). However, the role of Cartilage oligomeric matrix protein (COMP) in the development of hypoxia-induced PH is largely unknown. We tested the hypothesis that COMP deficiency induced by hypoxia leads to the phenotype switching of pulmonary arterial smooth muscle cells (PASMCs). The expression of COMP decreased in a chronic hypoxia rat PH model (P<0.05) and in PASMCs under hypoxia (3%O2) (P< 0.05). The expressions of differentiated marker proteins reduced in the pulmonary arteries from 5 month old COMP(-/...
Source: The International Journal of Biochemistry and Cell Biology - August 28, 2017 Category: Biochemistry Authors: Yu H, Jia Q, Feng X, Chen H, Wang L, Ni X, Kong W Tags: Int J Biochem Cell Biol Source Type: research

Two-pore channels mediated receptor-operated Ca2+ entry in pulmonary artery smooth muscle cells in response to hypoxia.
In conclusion, the TPCs influence on function of pulmonary artery smooth muscle cells by mediated Ca2+ Signals under hypoxia condition. PMID: 29355755 [PubMed - as supplied by publisher]
Source: The International Journal of Biochemistry and Cell Biology - January 17, 2018 Category: Biochemistry Authors: Jiang Y, Zhou Y, Peng G, Tian H, Pan D, Liu L, Yang X, Li C, Li W, Chen L, Ran P, Dai A Tags: Int J Biochem Cell Biol Source Type: research

Acute Intermittent Porphyria Causes Hepatic Mitochondrial Energetic Failure In A Mouse Model.
Abstract Acute intermittent porphyria (AIP), an inherited hepatic disorder, is due to a defect of hydroxymethylbilane synthase (HMBS), an enzyme involved in heme biosynthesis. AIP is characterized by recurrent, life-threatening attacks at least partly due to the increased hepatic production of 5-aminolaevulinic acid (ALA). Both the mitochondrial enzyme, ALA synthase (ALAS) 1, involved in the first step of heme biosynthesis, which is closely linked to mitochondrial bioenergetic pathways, and the promise of an ALAS1 siRNA hepatic therapy in humans, led us to investigate hepatic energetic metabolism in Hmbs KO mice t...
Source: The International Journal of Biochemistry and Cell Biology - April 10, 2014 Category: Biochemistry Authors: Homedan C, Laafi J, Schmitt C, Gueguen N, Lefebvre T, Karim Z, Desquiret-Dumas V, Wetterwald C, Deybach JC, Gouya L, Puy H, Reynier P, Malthièry Y Tags: Int J Biochem Cell Biol Source Type: research

Involvement of the AMPK-PTEN pathway in insulin resistance induced by high glucose in cultured rat podocytes.
Abstract As part of the filtration barrier, podocytes play an important role in the development of diabetic nephropathy. Disturbances in insulin signaling accompanied by insulin resistance can lead to various intracellular events. We hypothesized that high glucose concentrations would lead to disturbances in interactions between AMPK and PTEN proteins in podocytes. Experiments were performed in primary rat podocytes cultured with normal (5.6mM) or high (30mM) glucose concentrations for 5 d. Immunodetection methods were used to detect AMPK, PTEN, insulin receptor, and Akt proteins, and their phosphorylated forms. I...
Source: The International Journal of Biochemistry and Cell Biology - April 15, 2014 Category: Biochemistry Authors: Rogacka D, Piwkowska A, Audzeyenka I, Angielski S, Jankowski M Tags: Int J Biochem Cell Biol Source Type: research

Ataxia telangiectasia mutated inhibits oxidative stress-induced apoptosis by regulating heme oxygenase-1 expression.
In conclusion, ATM induces HO-1 expression via activation of PKC-δ and NF-κB and inhibits oxidative stress-induced apoptosis. A loss of HO-1 induction may explain why AT patients are vulnerable to oxidative stress. PMID: 25592228 [PubMed - as supplied by publisher]
Source: The International Journal of Biochemistry and Cell Biology - January 12, 2015 Category: Biochemistry Authors: Yu JH, Cho SO, Lim JW, Kim N, Kim H Tags: Int J Biochem Cell Biol Source Type: research

TLR2-MyD88-NF-κB pathway is involved in tubulointerstitial inflammation caused by proteinuria.
In this study, we hypothesized whether the activation of the TLR2-MyD88-NF-κB pathway is involved in tubulointerstitial inflammation induced by proteinuria. We observed expression of TLR2, MyD88, NF-κB, as well as TNF-α and IL-6 detected by immunohistostaining, Western blotting and real-time PCR in albumin-overloaded (AO) nephropathy rats. In vitro, we observed these markers in HK-2 cells stimulated by albumin. We used TLR2 siRNA or the NF-κB inhibitor BAY 11-7082 to observe the influence of TNF-α and IL-6 expression caused by albumin overload. Finally, we studied these markers in non-IgA mesangioproliferative glomeru...
Source: The International Journal of Biochemistry and Cell Biology - October 17, 2015 Category: Biochemistry Authors: Ding LH, Liu D, Xu M, Wu M, Liu H, Tang RN, Ma KL, Chen PS, Liu BC Tags: Int J Biochem Cell Biol Source Type: research

Inhibitory effects of Omega-3 fatty acids on Early Brain Injury after Subarachnoid Hemorrhage in Rats: possible involvement of G protein-coupled receptor 120/β-arrestin2/TGF-β activated kinase-1 binding protein-1 signaling pathway.
This study was to examine the effects of omega-3 fatty acids on SAH-induced EBI. Two weeks before SAH, 30% Omega-3 fatty acids was administered by oral gavage at 1g/kg body weight once every 24hours. Specific siRNA for GPR120 was exploited. Terminal deoxynucleotidyl transferase dUTP nick end labeling, fluoro-Jade B staining, and neurobehavioral scores and brain water content test showed that omega-3 fatty acids effectively suppressed SAH-induced brain cell apoptosis and neuronal degradation, behavioral impairment, and brain edema. Western blot, immunoprecipitation, and electrophoretic mobility shift assays results showed t...
Source: The International Journal of Biochemistry and Cell Biology - March 17, 2016 Category: Biochemistry Authors: Yin J, Li H, Meng C, Chen D, Chen Z, Wang Y, Wang Z, Chen G Tags: Int J Biochem Cell Biol Source Type: research

G9a inhibition induced PKM2 regulates autophagic responses.
Abstract Epigenetic regulation by histone methyltransferase G9a is known to control autophagic responses. As the link between autophagy and metabolic homeostasis is widely accepted, we investigated whether G9a affects metabolic circuitries to affect autophagic response in glioma cells. Both pharmacological inhibition and siRNA mediated knockdown of G9a increased autophagy marker LC3B in glioma cells. G9a inhibitor BIX-01294 (BIX) induced Akt-dependent increase in HIF-1α expression and activity. Inhibition of Akt-HIF-1α axis reversed BIX-mediated (i) increase in LC3B expression and (ii) decrease in Yes-associated...
Source: The International Journal of Biochemistry and Cell Biology - July 10, 2016 Category: Biochemistry Authors: Ahmad F, Dixit D, Joshi SD, Sen E Tags: Int J Biochem Cell Biol Source Type: research

Inhibiting post-translational core fucosylation prevents vascular calcification in the model of uremia.
In conclusion, this study provides evidence to suggest core fucosylation plays a major role in the process of VC and appropriate blockade of core fucosylation may represent a potential therapeutic strategy for treating VC in end-stage renal disease. PMID: 27521658 [PubMed - as supplied by publisher]
Source: The International Journal of Biochemistry and Cell Biology - August 9, 2016 Category: Biochemistry Authors: Wen X, Liu A, Yu C, Wang L, Zhou M, Wang N, Fang M, Wang W, Lin H Tags: Int J Biochem Cell Biol Source Type: research

Decrease in acrolein toxicity based on the decline of polyamine oxidases.
Abstract We have shown recently that acrolein is strongly involved in cell damage during brain infarction and chronic renal failure. To study the mechanism of acrolein detoxification, we tried to isolate Neuro2a cells with reduced sensitivity to acrolein toxicity (Neuro2a-ATD cells). In one cell line, Neuro2a-ATD1, the level of glutathione (GSH) was increased. We recently isolated a second cell line, Neuro2a-ATD2, and found that acrolein-producing enzymes [polyamine oxidases (PAO); i.e. acetylpolyamine oxidase (AcPAO), and spermine oxidase (SMO)] are reduced in this cell line due to changes at the level of transcr...
Source: The International Journal of Biochemistry and Cell Biology - August 29, 2016 Category: Biochemistry Authors: Uemura T, Nakamura M, Sakamoto A, Suzuki T, Dohmae N, Terui Y, Tomitori H, Casero RA, Kashiwagi K, Igarashi K Tags: Int J Biochem Cell Biol Source Type: research

Sp1 is a Competitive Endogenous RNA of Klf4 during Odontoblast Differentiation.
In this study, we predicted a group of potential Klf4 ceRNAs with bioinformatics approach, and examined the expression of Klf4 and five interested potential ceRNAs including Sp1 using real-time PCR during odontoblastic differentiation of mDPC6T. The expression levels of both Sp1 and Klf4 were significantly upregulated during this process. In situ hybridization verified that Sp1 was co-expressed with Klf4 in the differentiating and the mature odontoblasts in vivo. Knockdown of Sp1 using siRNA resulted in a significant reduction of Klf4 and vice visa. This interaction was further confirmed to be miRNA dependent. Common miRNA...
Source: The International Journal of Biochemistry and Cell Biology - February 22, 2017 Category: Biochemistry Authors: Zhang J, Liu H, Lin H, Li S, Tao H, Zhang L, Yuan G, Chen Z Tags: Int J Biochem Cell Biol Source Type: research