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10.1152/ajprenal.00580.2007 http://scihub22266oqcxt.onion/10.1152/ajprenal.00580.2007 C4067119!4067119 !19261744     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=19261744 &cmd=llinks): Failed to open stream: HTTP request failed! 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Angiotensin II type 1 receptor blocker attenuates the activation of ERK and NADPH oxidase by mechanical strain in mesangial cells in the absence of angiotensin II |pdf=|usr=}}{{19261744 }} gab.com Text Angiotensin II type 1 receptor blocker attenuates the activation of ERK and NADPH oxidase by mechanical strain in mesangial cells in the absence of angiotensin II JO: Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=19261744 #FOAvip It has been reported that mechanical strain activates extracellular signal-regulated protein kinases (ERK) without the involvement of angiotensin II (Ang II) in cardiomyocytes. We examined the effects of mechanical strain on ERK phosphorylation levels in the absence of Ang II using rat mesangial cells. The ratio of phosphorylated ERK (p-ERK) to total ERK expression was increased by cyclic mechanical strain in a time- and elongation strength-dependent manner. With olmesartan [Ang II type 1 receptor (AT1R) antagonist] pretreatment, p-ERK plateau levels decreased in a dose-dependent manner (EC(50) = 1.3 x 10(-8) M, maximal inhibition 50.6 +/- 11.0% at 10(-5) M); a similar effect was observed with RNA interference against Ang II type 1A receptor (AT(1A)R) and Tempol, a superoxide dismutase mimetic. In addition to the inhibition of p-ERK levels, olmesartan blocked the increase in cell surface and phosphorylated p47(phox) induced by mechanical strain and also lowered the mRNA expression levels of NADPH oxidase subunits. These results demonstrate that mechanical strain stimulates AT1R to phosphorylate ERK in mesangial cells in the absence of Ang II. This mechanotransduction mechanism is involved in the oxidative stress caused by NADPH oxidase and is blocked by olmesartan. The inverse agonistic activity of this AT1R blocker may be useful for the prevention of mesangial proliferation and renal damage caused by mechanical strain/oxidative stress regardless of circulating or tissue Ang II levels. Twit Text FOAVip Angiotensin II type 1 receptor blocker attenuates the activation of ERK and NADPH oxidase by mechanical strain in mesangial cells in the absence of angiotensin II ????Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=19261744 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=19261744 #FOAvip English Wikipedia <ref>{{Cite pmid|19261744 }}</ref> Angiotensin II type 1 receptor blocker attenuates the activation of ERK and NADPH oxidase by mechanical strain in mesangial cells in the absence of angiotensin II #MMPMID19261744 Yatabe J ; Sanada H ; Yatabe MS ; Hashimoto S ; Yoneda M ; Felder RA ; Jose PA ; Watanabe T Am J Physiol Renal Physiol 2009[May]; 296 (5 ): F1052-60 PMID19261744 show ga It has been reported that mechanical strain activates extracellular signal-regulated protein kinases (ERK) without the involvement of angiotensin II (Ang II) in cardiomyocytes. We examined the effects of mechanical strain on ERK phosphorylation levels in the absence of Ang II using rat mesangial cells. The ratio of phosphorylated ERK (p-ERK) to total ERK expression was increased by cyclic mechanical strain in a time- and elongation strength-dependent manner. With olmesartan [Ang II type 1 receptor (AT1R) antagonist] pretreatment, p-ERK plateau levels decreased in a dose-dependent manner (EC(50) = 1.3 x 10(-8) M, maximal inhibition 50.6 +/- 11.0% at 10(-5) M); a similar effect was observed with RNA interference against Ang II type 1A receptor (AT(1A)R) and Tempol, a superoxide dismutase mimetic. In addition to the inhibition of p-ERK levels, olmesartan blocked the increase in cell surface and phosphorylated p47(phox) induced by mechanical strain and also lowered the mRNA expression levels of NADPH oxidase subunits. These results demonstrate that mechanical strain stimulates AT1R to phosphorylate ERK in mesangial cells in the absence of Ang II. This mechanotransduction mechanism is involved in the oxidative stress caused by NADPH oxidase and is blocked by olmesartan. The inverse agonistic activity of this AT1R blocker may be useful for the prevention of mesangial proliferation and renal damage caused by mechanical strain/oxidative stress regardless of circulating or tissue Ang II levels. |Angiotensin II Type 1 Receptor Blockers/*pharmacology [MESH] |Angiotensin II/pharmacology [MESH] |Animals [MESH] |Autocrine Communication/drug effects/physiology [MESH] |Cells, Cultured [MESH] |Chelating Agents/pharmacology [MESH] |Cytochalasin D/pharmacology [MESH] |Egtazic Acid/analogs & derivatives/pharmacology [MESH] |Extracellular Signal-Regulated MAP Kinases/*metabolism [MESH] |Gene Expression/drug effects/physiology [MESH] |Hypertension, Renal/drug therapy/metabolism/physiopathology [MESH] |Imidazoles/*pharmacology [MESH] |Male [MESH] |Mesangial Cells/cytology/*drug effects/*enzymology [MESH] |MicroRNAs/pharmacology [MESH] |NADH, NADPH Oxidoreductases/*metabolism [MESH] |NADPH Oxidase 1 [MESH] |Nucleic Acid Synthesis Inhibitors/pharmacology [MESH] |Oxidative Stress/physiology [MESH] |Paracrine Communication/drug effects/physiology [MESH] |Phosphorylation/physiology [MESH] |Rats [MESH] |Rats, Sprague-Dawley [MESH] |Receptor, Angiotensin, Type 1/genetics/metabolism [MESH] |Stress, Mechanical [MESH] |Tetrazoles/*pharmacology [MESH]Angiotensin II type 1 receptor blocker attenuates the activation of ER(epmc).pdf DeepDyve Pubget Overpricing