Asymmetric dimethyl arginine induces pulmonary vascular dysfunction via activation of signal transducer and activator of transcription 3 and stabilization of hypoxia-inducible factor 1-alpha

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00159816%3A_____%2F15%3A00063065" target="_blank" >RIV/00159816:_____/15:00063065 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/68081707:_____/15:00455893

Výsledek na webu

<a href="http://dx.doi.org/10.1016/j.vph.2015.06.005" target="_blank" >http://dx.doi.org/10.1016/j.vph.2015.06.005</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.vph.2015.06.005" target="_blank" >10.1016/j.vph.2015.06.005</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Asymmetric dimethyl arginine induces pulmonary vascular dysfunction via activation of signal transducer and activator of transcription 3 and stabilization of hypoxia-inducible factor 1-alpha

Popis výsledku v původním jazyce

Pulmonary hypertension (PH), associated with imbalance in vasoactive mediators and massive remodeling of pulmonary vasculature, represents a serious health complication. Despite the progress in treatment, PH patients typically have poor prognoses with severely affected quality of life. Asymmetric dimethyl arginine (ADMA), endogenous inhibitor of endothelial nitric oxide synthase (eNOS), also represents one of the critical regulators of pulmonary vascular functions. The present study describes a novel mechanism of ADMA-induced dysfunction in human pulmonary endothelial and smooth muscle cells. The effect of ADMA was compared with well-established model of hypoxia-induced pulmonary vascular dysfunction. It was discovered for the first time that ADMA induced the activation of signal transducer and activator of transcription 3 (STAT3) and stabilization of hypoxia inducible factor 1? (HIF-1?) in both types of cells, associated with drastic alternations in normal cellular functions (e.g., ni

Název v anglickém jazyce

Asymmetric dimethyl arginine induces pulmonary vascular dysfunction via activation of signal transducer and activator of transcription 3 and stabilization of hypoxia-inducible factor 1-alpha

Popis výsledku anglicky

Pulmonary hypertension (PH), associated with imbalance in vasoactive mediators and massive remodeling of pulmonary vasculature, represents a serious health complication. Despite the progress in treatment, PH patients typically have poor prognoses with severely affected quality of life. Asymmetric dimethyl arginine (ADMA), endogenous inhibitor of endothelial nitric oxide synthase (eNOS), also represents one of the critical regulators of pulmonary vascular functions. The present study describes a novel mechanism of ADMA-induced dysfunction in human pulmonary endothelial and smooth muscle cells. The effect of ADMA was compared with well-established model of hypoxia-induced pulmonary vascular dysfunction. It was discovered for the first time that ADMA induced the activation of signal transducer and activator of transcription 3 (STAT3) and stabilization of hypoxia inducible factor 1? (HIF-1?) in both types of cells, associated with drastic alternations in normal cellular functions (e.g., ni

Druh

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

CEP obor

FR - Farmakologie a lékárnická chemie

OECD FORD obor

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Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2015

Kód důvěrnosti údajů

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

Název periodika

Vascular Pharmacology

ISSN

1537-1891

e-ISSN

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Svazek periodika

73

Číslo periodika v rámci svazku

OCT

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

11

Strana od-do

138-148

Kód UT WoS článku

000362056600018

EID výsledku v databázi Scopus

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