Atorvastatin-induced endothelial nitric oxide synthase expression in endothelial cells is mediated by endoglin

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11160%2F15%3A10312714" target="_blank" >RIV/00216208:11160/15:10312714 - isvavai.cz</a>

Výsledek na webu

<a href="http://www.jpp.krakow.pl/journal/archive/06_15/pdf/403_06_15_article.pdf" target="_blank" >http://www.jpp.krakow.pl/journal/archive/06_15/pdf/403_06_15_article.pdf</a>

DOI - Digital Object Identifier

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Jazyk výsledku

angličtina

Název v původním jazyce

Atorvastatin-induced endothelial nitric oxide synthase expression in endothelial cells is mediated by endoglin

Popis výsledku v původním jazyce

Endoglin, a transforming growth factor beta (TGF-beta) receptor type III, is co-expressed with endothelial nitric oxide synthase (eNOS) in aortic endothelium in atherosclerotic plaques of mice. Interestingly, atorvastatin (ATV) is able to increase both endoglin and eNOS expression and reduce plaque size beyond its lipid lowering effects but by unknown mechanisms. We hypothesized whether inflammation modulates ATV-dependent induction of endoglin and eNOS expression in vitro in endothelial cells and whether ATV-induced eNOS expression is regulated via endoglin. After treatment of human umbilical vein endothelial cells (HUVECs) with TNF-alpha, endoglin and eNOS protein expression was reduced, concomitantly with increased levels of cell surface VCAM-1 andsoluble endoglin, as determined by flow cytometry, Western blot and ELISA analyses. By contrast, ATV treatment increased endoglin and eNOS protein expression, while preventing TNF-alpha-mediated downregulation of endoglin and eNOS protein

Název v anglickém jazyce

Atorvastatin-induced endothelial nitric oxide synthase expression in endothelial cells is mediated by endoglin

Popis výsledku anglicky

Endoglin, a transforming growth factor beta (TGF-beta) receptor type III, is co-expressed with endothelial nitric oxide synthase (eNOS) in aortic endothelium in atherosclerotic plaques of mice. Interestingly, atorvastatin (ATV) is able to increase both endoglin and eNOS expression and reduce plaque size beyond its lipid lowering effects but by unknown mechanisms. We hypothesized whether inflammation modulates ATV-dependent induction of endoglin and eNOS expression in vitro in endothelial cells and whether ATV-induced eNOS expression is regulated via endoglin. After treatment of human umbilical vein endothelial cells (HUVECs) with TNF-alpha, endoglin and eNOS protein expression was reduced, concomitantly with increased levels of cell surface VCAM-1 andsoluble endoglin, as determined by flow cytometry, Western blot and ELISA analyses. By contrast, ATV treatment increased endoglin and eNOS protein expression, while preventing TNF-alpha-mediated downregulation of endoglin and eNOS protein

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

FA - Kardiovaskulární nemoci včetně kardiochirurgie

OECD FORD obor

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Projekt

<a href="/cs/project/EE2.3.30.0061" target="_blank" >EE2.3.30.0061: Zvýšení kapacity vědecko-výzkumných týmů Univerzity Karlovy prostřednictvím nových pozic pro absolventy doktorandských studií</a><br>

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)<br>S - Specificky vyzkum na vysokych skolach<br>I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2015

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Journal of Physiology and Pharmacology

ISSN

0867-5910

e-ISSN

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Svazek periodika

66

Číslo periodika v rámci svazku

3

Stát vydavatele periodika

PL - Polská republika

Počet stran výsledku

11

Strana od-do

403-413

Kód UT WoS článku

000357361400009

EID výsledku v databázi Scopus

2-s2.0-84930901347