Mechanism of the susceptibility of remodeled pulmonary vessels to drug-induced cell killing

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00064190%3A_____%2F14%3A%230001019" target="_blank" >RIV/00064190:_____/14:#0001019 - isvavai.cz</a>

Výsledek na webu

<a href="http://dx.doi.org/10.1161/JAHA.113.000520" target="_blank" >http://dx.doi.org/10.1161/JAHA.113.000520</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1161/JAHA.113.000520" target="_blank" >10.1161/JAHA.113.000520</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Mechanism of the susceptibility of remodeled pulmonary vessels to drug-induced cell killing

Popis výsledku v původním jazyce

Pulmonary arterial hypertension remains a devastating disease without a cure. The major complication of this disease is the abnormal growth of vascular cells, resulting in pulmonary vascular remodeling. Thus, agents, which affect the remodeled vessels bykilling unwanted cells, should improve treatment strategies. The present study reports that antitumor drugs selectively kill vascular cells in remodeled pulmonary vessels in rat models of pulmonary hypertension. METHODS AND RESULTS: After developing pulmonary vascular remodeling in chronic hypoxia or chronic hypoxia/SU-5416 models, rats were injected with antitumor drugs including proteasome inhibitors (bortezomib and MG-132) and daunorubicin. Within 1 to 3 days, these agents reduced the media and intima thickness of remodeled pulmonary vascular walls, but not the thickness of normal pulmonary vessels. These drugs also promoted apoptotic and autophagic death of vascular cells in the remodeled vessels, but not in normal vessels. We prov

Název v anglickém jazyce

Mechanism of the susceptibility of remodeled pulmonary vessels to drug-induced cell killing

Popis výsledku anglicky

Pulmonary arterial hypertension remains a devastating disease without a cure. The major complication of this disease is the abnormal growth of vascular cells, resulting in pulmonary vascular remodeling. Thus, agents, which affect the remodeled vessels bykilling unwanted cells, should improve treatment strategies. The present study reports that antitumor drugs selectively kill vascular cells in remodeled pulmonary vessels in rat models of pulmonary hypertension. METHODS AND RESULTS: After developing pulmonary vascular remodeling in chronic hypoxia or chronic hypoxia/SU-5416 models, rats were injected with antitumor drugs including proteasome inhibitors (bortezomib and MG-132) and daunorubicin. Within 1 to 3 days, these agents reduced the media and intima thickness of remodeled pulmonary vascular walls, but not the thickness of normal pulmonary vessels. These drugs also promoted apoptotic and autophagic death of vascular cells in the remodeled vessels, but not in normal vessels. We prov

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

—

Návaznosti

V - Vyzkumna aktivita podporovana z jinych verejnych zdroju

Rok uplatnění

2014

Kód důvěrnosti údajů

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

Název periodika

Journal of the American Heart Association

ISSN

2047-9980

e-ISSN

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Svazek periodika

3

Číslo periodika v rámci svazku

1

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

1

Strana od-do

"e000520"

Kód UT WoS článku

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EID výsledku v databázi Scopus

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