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High glucose-induced oxidative stress increases transient receptor potential channel expression in human monocytes |pdf=|usr=}}{{20068131 }} gab.com Text High glucose-induced oxidative stress increases transient receptor potential channel expression in human monocytes JO: Diabetes http://www.kidney.de/pget.php?&tw=1&pmid=20068131 #FOAvip OBJECTIVE: Transient receptor potential (TRP) channel-induced cation influx activates human monocytes, which play an important role in the pathogenesis of atherosclerosis. In the present study, we investigated the effects of high glucose-induced oxidative stress on TRP channel expression in human monocytes. RESEARCH DESIGN AND METHODS: Human monocytes were exposed to control conditions (5.6 mmol/l d-glucose), high glucose (30 mmol/l d-glucose or l-glucose), 100 micromol/l peroxynitrite, or high glucose in the presence of the superoxide dismutase mimetic tempol (100 micromol/l). TRP mRNA and TRP protein expression was measured using quantitative real-time RT-PCR and quantitative in-cell Western assay, respectively. Calcium influx and intracellular reactive oxygen species were measured using fluorescent dyes. RESULTS: Administration of high d-glucose significantly increased reactive oxygen species. High d-glucose or peroxynitrite significantly increased the expression of TRP canonical type 1 (TRPC1), TRPC3, TRPC5, TRPC6, TRP melastatin type 6 (TRPM6), and TRPM7 mRNA and TRPC3 and TRPC6 proteins. High d-glucose plus tempol or high l-glucose did not affect TRP expression. Increased oxidative stress by lipopolysaccharide or tumor necrosis factor-alpha increased TRP mRNA expression, whereas the reduction of superoxide radicals using diphenylene iodonium significantly reduced TRP mRNA expression. Increased TRPC3 and TRPC6 protein expression was accompanied by increased 1-oleoyl-2-acetyl-sn-glycerol-induced calcium influx, which was blocked by the TRPC inhibitor 2-aminoethoxydiphenylborane. TRPC6 mRNA was significantly higher in monocytes from 18 patients with type 2 diabetes compared with 28 control subjects (P < 0.05). CONCLUSIONS: High d-glucose-induced oxidative stress increases TRP expression and calcium influx in human monocytes, pointing to a novel pathway for increased activation of monocytes and hence atherosclerosis in patients with diabetes. Twit Text FOAVip High glucose-induced oxidative stress increases transient receptor potential channel expression in human monocytes ????Diabetes http://www.kidney.de/pget.php?&tw=1&pmid=20068131 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=20068131 #FOAvip English Wikipedia <ref>{{Cite pmid|20068131 }}</ref> High glucose-induced oxidative stress increases transient receptor potential channel expression in human monocytes #MMPMID20068131 Wuensch T ; Thilo F ; Krueger K ; Scholze A ; Ristow M ; Tepel M Diabetes 2010[Apr]; 59 (4 ): 844-9 PMID20068131 show ga OBJECTIVE: Transient receptor potential (TRP) channel-induced cation influx activates human monocytes, which play an important role in the pathogenesis of atherosclerosis. In the present study, we investigated the effects of high glucose-induced oxidative stress on TRP channel expression in human monocytes. RESEARCH DESIGN AND METHODS: Human monocytes were exposed to control conditions (5.6 mmol/l d-glucose), high glucose (30 mmol/l d-glucose or l-glucose), 100 micromol/l peroxynitrite, or high glucose in the presence of the superoxide dismutase mimetic tempol (100 micromol/l). TRP mRNA and TRP protein expression was measured using quantitative real-time RT-PCR and quantitative in-cell Western assay, respectively. Calcium influx and intracellular reactive oxygen species were measured using fluorescent dyes. RESULTS: Administration of high d-glucose significantly increased reactive oxygen species. High d-glucose or peroxynitrite significantly increased the expression of TRP canonical type 1 (TRPC1), TRPC3, TRPC5, TRPC6, TRP melastatin type 6 (TRPM6), and TRPM7 mRNA and TRPC3 and TRPC6 proteins. High d-glucose plus tempol or high l-glucose did not affect TRP expression. Increased oxidative stress by lipopolysaccharide or tumor necrosis factor-alpha increased TRP mRNA expression, whereas the reduction of superoxide radicals using diphenylene iodonium significantly reduced TRP mRNA expression. Increased TRPC3 and TRPC6 protein expression was accompanied by increased 1-oleoyl-2-acetyl-sn-glycerol-induced calcium influx, which was blocked by the TRPC inhibitor 2-aminoethoxydiphenylborane. TRPC6 mRNA was significantly higher in monocytes from 18 patients with type 2 diabetes compared with 28 control subjects (P < 0.05). CONCLUSIONS: High d-glucose-induced oxidative stress increases TRP expression and calcium influx in human monocytes, pointing to a novel pathway for increased activation of monocytes and hence atherosclerosis in patients with diabetes. |DNA Primers [MESH] |Gene Expression Regulation/drug effects [MESH] |Glucose/*pharmacology [MESH] |Humans [MESH] |Monocytes/drug effects/*physiology [MESH] |Oxidative Stress/drug effects/*physiology [MESH] |Peroxynitrous Acid/pharmacology [MESH] |RNA, Messenger/*genetics [MESH] |RNA-Directed DNA Polymerase [MESH] |RNA/genetics/isolation & purification [MESH] |Reactive Oxygen Species/metabolism [MESH] |Reverse Transcriptase Polymerase Chain Reaction [MESH] |TRPC Cation Channels/*genetics [MESH]High glucose-induced oxidative stress increases transient receptor pot(epmc).pdf DeepDyve Pubget Overpricing