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10.1016/j.bbamcr.2014.02.009 http://scihub22266oqcxt.onion/10.1016/j.bbamcr.2014.02.009 C4086191!4086191!24576409     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Biochim+Biophys+Acta 2014 ; 1843 (6): 1063-75 Nephropedia Template TP {{tp|p=24576409|t=2014. Mechanism of endoplasmic reticulum stress-induced vascular endothelial dysfunction |pdf=|usr=}}{{24576409}} gab.com Text Mechanism of endoplasmic reticulum stress-induced vascular endothelial dysfunction JO: Biochim Biophys Acta http://www.kidney.de/pget.php?&tw=1&pmid=24576409 #FOAvip Background: We recently reported that ER stress plays a key role in vascular endothelial dysfunction during hypertension. In this study we aimed to elucidate the mechanisms by which ER stress induction and oxidative stress impair vascular endothelial function. Methodology/Principal findings: we conducted in vitro studies with primary endothelial cells from coronary arteries stimulated with tunicamycin, 1 ?g/mL, in the presence or absence of two ER stress inhibitors: tauroursodeoxycholic acid (Tudca), 500 ?g/mL, and 4-phenyl butyric acid (PBA), 5 mM. ER stress induction was assessed by enhanced phosphorylation of PERK and eIF2?, and increased expression of CHOP, ATF6 and Grp78/Bip. The ER stress induction increased p38 MAPK phosphorylation, Nox2/4 mRNA levels and NADPH oxidase activity, decreased eNOS promoter activity, eNOS expression and phosphorylation, and nitrite levels. Interestingly, the inhibition of p38 MAPK pathway reduced CHOP and Bip expression enhanced by tunicamycin and restored eNOS promoter activation as well as phosphorylation. To study the effects of ER stress induction in vivo, we used C57BL/6J mice and p47phox?/? mice injected with tunicamycin or saline. The ER stress induction in mice significantly impaired vascular endothelium-dependent and independent relaxation in C57BL/6J mice compared with p47phox?/? mice indicating NADPH oxidase activity as an intermediate for ER stress in vascular endothelial dysfunction. Conclusion/Significance: We conclude that chemically induced ER stress leads to a downstream enhancement of p38 MAPK and oxidative stress causing vascular endothelial dysfunction. Our results indicate that inhibition of ER stress could be a novel therapeutic strategy to attenuate vascular dysfunction during cardiovascular diseases. Twit Text FOAVip Mechanism of endoplasmic reticulum stress-induced vascular endothelial dysfunction ????Biochim Biophys Acta http://www.kidney.de/pget.php?&tw=1&pmid=24576409 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24576409 #FOAvip English Wikipedia <ref>{{Cite pmid|24576409}}</ref> Mechanism of endoplasmic reticulum stress-induced vascular endothelial dysfunction #MMPMID24576409 Galán M; Kassan M; Kadowitz PJ; Trebak M; Belmadani S; Matrougui K Biochim Biophys Acta 2014[Jun]; 1843 (6): 1063-75 PMID24576409show ga Background: We recently reported that ER stress plays a key role in vascular endothelial dysfunction during hypertension. In this study we aimed to elucidate the mechanisms by which ER stress induction and oxidative stress impair vascular endothelial function. Methodology/Principal findings: we conducted in vitro studies with primary endothelial cells from coronary arteries stimulated with tunicamycin, 1 ?g/mL, in the presence or absence of two ER stress inhibitors: tauroursodeoxycholic acid (Tudca), 500 ?g/mL, and 4-phenyl butyric acid (PBA), 5 mM. ER stress induction was assessed by enhanced phosphorylation of PERK and eIF2?, and increased expression of CHOP, ATF6 and Grp78/Bip. The ER stress induction increased p38 MAPK phosphorylation, Nox2/4 mRNA levels and NADPH oxidase activity, decreased eNOS promoter activity, eNOS expression and phosphorylation, and nitrite levels. Interestingly, the inhibition of p38 MAPK pathway reduced CHOP and Bip expression enhanced by tunicamycin and restored eNOS promoter activation as well as phosphorylation. To study the effects of ER stress induction in vivo, we used C57BL/6J mice and p47phox?/? mice injected with tunicamycin or saline. The ER stress induction in mice significantly impaired vascular endothelium-dependent and independent relaxation in C57BL/6J mice compared with p47phox?/? mice indicating NADPH oxidase activity as an intermediate for ER stress in vascular endothelial dysfunction. Conclusion/Significance: We conclude that chemically induced ER stress leads to a downstream enhancement of p38 MAPK and oxidative stress causing vascular endothelial dysfunction. Our results indicate that inhibition of ER stress could be a novel therapeutic strategy to attenuate vascular dysfunction during cardiovascular diseases. äMechanism of endoplasmic reticulum stress-induced vascular endothelial(epmc).pdf DeepDyve Pubget Overpricing