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| rdf:type
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| Description
| - Ischemie-reperfuze (I/R) vede k vážným komplikacím v důsledku odumírání kardiomyocytů. Použili jsme kardiomyocytům podobnou buněčnou linii H9c2, abychom studovali mechanismus buněčného poškození. Vystavení buněk simulované I/R vedlo k jejich apoptóze. Zvýšená exprese Bcl-2 a Bcl-xL chránila buňky před apoptózou, zatímco zvýšená exprese Bax je činila citlivými k indukci programované buněčné smrti. Koenzym Q cílený do mitochondrií (mitoQ) a superoxiddismutáza inhibovaly akumulaci ROS a indukci apoptózy. mtDNA-deficientní buňky odpovídaly na I/R sníženým vznikem ROS a sníženou apoptózou. Bylo zjištěno, že apoptóza nastávala během reperfuze následující ischemii a že zotavení bylo lepší pokud myším srdcím byl dodán mitoQ. Závěrem lze říci, že I/R způsobí apoptózu v kultivovaných kardiomyocytech i srdeční tkáni hlavně cestou vzniku superoxidu pocházejícího z mitochondrií s následnou apoptózou během reperfuzní fáze. (cs)
- 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 hearts from 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.
- 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 hearts from 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. (en)
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| Title
| - Mitochondria transmit apoptosis signalling in cardiomyocyte-like cells and isolated hearts exposed to experimental ischemia-reperfusion injury
- Mitochondria transmit apoptosis signalling in cardiomyocyte-like cells and isolated hearts exposed to experimental ischemia-reperfusion injury (en)
- Mitochondrie přenášejí signály apoptózy v buňkách podobným kardiomyocytům a izolovaných srdcích vystavených experimentální ischemii-reperfusi (cs)
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| skos:prefLabel
| - Mitochondria transmit apoptosis signalling in cardiomyocyte-like cells and isolated hearts exposed to experimental ischemia-reperfusion injury
- Mitochondria transmit apoptosis signalling in cardiomyocyte-like cells and isolated hearts exposed to experimental ischemia-reperfusion injury (en)
- Mitochondrie přenášejí signály apoptózy v buňkách podobným kardiomyocytům a izolovaných srdcích vystavených experimentální ischemii-reperfusi (cs)
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| skos:notation
| - RIV/68378050:_____/07:00096817!RIV08-AV0-68378050
|
| http://linked.open.../vavai/riv/strany
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| http://linked.open...avai/riv/aktivita
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| http://linked.open...avai/riv/aktivity
| - Z(AV0Z50520514), Z(AV0Z50520701)
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| http://linked.open...iv/cisloPeriodika
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| http://linked.open...vai/riv/dodaniDat
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| http://linked.open...aciTvurceVysledku
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| http://linked.open.../riv/druhVysledku
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| http://linked.open...iv/duvernostUdaju
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| http://linked.open...titaPredkladatele
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| http://linked.open...dnocenehoVysledku
| |
| http://linked.open...ai/riv/idVysledku
| - RIV/68378050:_____/07:00096817
|
| http://linked.open...riv/jazykVysledku
| |
| http://linked.open.../riv/klicovaSlova
| - kardiomyocyty; superoxide; apoptosis (en)
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| http://linked.open.../riv/klicoveSlovo
| |
| http://linked.open...odStatuVydavatele
| - GB - Spojené království Velké Británie a Severního Irska
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| http://linked.open...ontrolniKodProRIV
| |
| http://linked.open...i/riv/nazevZdroje
| |
| http://linked.open...in/vavai/riv/obor
| |
| http://linked.open...ichTvurcuVysledku
| |
| http://linked.open...cetTvurcuVysledku
| |
| http://linked.open...UplatneniVysledku
| |
| http://linked.open...v/svazekPeriodika
| |
| http://linked.open...iv/tvurceVysledku
| - Neužil, Jiří
- Zobalová, Renata
- Witting, P. K.
- Swettenham, E.
- Gellert, N.
- Dalen, H.
- Dong, J. F.
- Wang, X. F.
- Headrick, J. P.
- Lidebjer, C.
- Widen, C.
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| http://linked.open...n/vavai/riv/zamer
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| issn
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| number of pages
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