Mitochondrie přenášejí signály apoptózy v buňkách podobným kardiomyocytům a izolovaných srdcích vystavených experimentální ischemii-reperfusi

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378050%3A_____%2F07%3A00096817" target="_blank" >RIV/68378050:_____/07:00096817 - isvavai.cz</a>

Výsledek na webu

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DOI - Digital Object Identifier

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Jazyk výsledku

angličtina

Název v původním jazyce

Mitochondria transmit apoptosis signalling in cardiomyocyte-like cells and isolated hearts exposed to experimental ischemia-reperfusion injury

Popis výsledku v původním jazyce

Ischemia-reperfusion is a condition leading to serious complications due to death of cardiac myocytes. We used cardiomyocyte-like cell line H9c2 to study the mechanism underlying cell damage. Exposure of cells to simulated I/R lead to their apoptosis. Overexpression of Bcl-2 and Bcl-xL protected cells from apoptosis while overexpression of Bax sensitized them to programmed cell death induction. Mitochondria-targeted coenzyme Q and superoxide dismutase both inhibited accumulation of ROS and apoptosis induction. Notably, mtDNA-deficient cells responded to I/R by decreased ROS generation and apoptosis. Using both in situ and in vivo approaches it was found that apoptosis occurred during reperfusion following ischemia and recovery was enhanced when heartsfrom mice were supplemented with mitoQ. In conclusion, I/R results in apoptosis in cultured cardiac myocytes and heart tissue largely via generation of mitochondria-derived superoxide, with ensuing apoptosis during the reperfusion phase.

Název v anglickém jazyce

Mitochondria transmit apoptosis signalling in cardiomyocyte-like cells and isolated hearts exposed to experimental ischemia-reperfusion injury

Popis výsledku anglicky

Ischemia-reperfusion is a condition leading to serious complications due to death of cardiac myocytes. We used cardiomyocyte-like cell line H9c2 to study the mechanism underlying cell damage. Exposure of cells to simulated I/R lead to their apoptosis. Overexpression of Bcl-2 and Bcl-xL protected cells from apoptosis while overexpression of Bax sensitized them to programmed cell death induction. Mitochondria-targeted coenzyme Q and superoxide dismutase both inhibited accumulation of ROS and apoptosis induction. Notably, mtDNA-deficient cells responded to I/R by decreased ROS generation and apoptosis. Using both in situ and in vivo approaches it was found that apoptosis occurred during reperfusion following ischemia and recovery was enhanced when heartsfrom mice were supplemented with mitoQ. In conclusion, I/R results in apoptosis in cultured cardiac myocytes and heart tissue largely via generation of mitochondria-derived superoxide, with ensuing apoptosis during the reperfusion phase.

Druh

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

CEP obor

EB - Genetika a molekulární biologie

OECD FORD obor

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Projekt

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Návaznosti

Z - Vyzkumny zamer (s odkazem do CEZ)

Rok uplatnění

2007

Kód důvěrnosti údajů

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

Název periodika

Redox Report

ISSN

1351-0002

e-ISSN

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Svazek periodika

12

Číslo periodika v rámci svazku

3

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

16

Strana od-do

148-162

Kód UT WoS článku

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EID výsledku v databázi Scopus

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