"Mitochondrie p\u0159en\u00E1\u0161ej\u00ED sign\u00E1ly apopt\u00F3zy v bu\u0148k\u00E1ch podobn\u00FDm kardiomyocyt\u016Fm a izolovan\u00FDch srdc\u00EDch vystaven\u00FDch experiment\u00E1ln\u00ED ischemii-reperfusi"@cs . "12" . . "Mitochondrie p\u0159en\u00E1\u0161ej\u00ED sign\u00E1ly apopt\u00F3zy v bu\u0148k\u00E1ch podobn\u00FDm kardiomyocyt\u016Fm a izolovan\u00FDch srdc\u00EDch vystaven\u00FDch experiment\u00E1ln\u00ED ischemii-reperfusi"@cs . . "Neu\u017Eil, Ji\u0159\u00ED" . "Lidebjer, C." . . "Mitochondria transmit apoptosis signalling in cardiomyocyte-like cells and isolated hearts exposed to experimental ischemia-reperfusion injury" . "kardiomyocyty; superoxide; apoptosis"@en . . "Ischemie-reperfuze (I/R) vede k v\u00E1\u017En\u00FDm komplikac\u00EDm v d\u016Fsledku odum\u00EDr\u00E1n\u00ED kardiomyocyt\u016F. Pou\u017Eili jsme kardiomyocyt\u016Fm podobnou bun\u011B\u010Dnou linii H9c2, abychom studovali mechanismus bun\u011B\u010Dn\u00E9ho po\u0161kozen\u00ED. Vystaven\u00ED bun\u011Bk simulovan\u00E9 I/R vedlo k jejich apopt\u00F3ze. Zv\u00FD\u0161en\u00E1 exprese Bcl-2 a Bcl-xL chr\u00E1nila bu\u0148ky p\u0159ed apopt\u00F3zou, zat\u00EDmco zv\u00FD\u0161en\u00E1 exprese Bax je \u010Dinila citliv\u00FDmi k indukci programovan\u00E9 bun\u011B\u010Dn\u00E9 smrti. Koenzym Q c\u00EDlen\u00FD do mitochondri\u00ED (mitoQ) a superoxiddismut\u00E1za inhibovaly akumulaci ROS a indukci apopt\u00F3zy. mtDNA-deficientn\u00ED bu\u0148ky odpov\u00EDdaly na I/R sn\u00ED\u017Een\u00FDm vznikem ROS a sn\u00ED\u017Eenou apopt\u00F3zou. Bylo zji\u0161t\u011Bno, \u017Ee apopt\u00F3za nast\u00E1vala b\u011Bhem reperfuze n\u00E1sleduj\u00EDc\u00ED ischemii a \u017Ee zotaven\u00ED bylo lep\u0161\u00ED pokud my\u0161\u00EDm srdc\u00EDm byl dod\u00E1n mitoQ. Z\u00E1v\u011Brem lze \u0159\u00EDci, \u017Ee I/R zp\u016Fsob\u00ED apopt\u00F3zu v kultivovan\u00FDch kardiomyocytech i srde\u010Dn\u00ED tk\u00E1ni hlavn\u011B cestou vzniku superoxidu poch\u00E1zej\u00EDc\u00EDho z mitochondri\u00ED s n\u00E1slednou apopt\u00F3zou b\u011Bhem reperfuzn\u00ED f\u00E1ze."@cs . "Swettenham, E." . "Mitochondria transmit apoptosis signalling in cardiomyocyte-like cells and isolated hearts exposed to experimental ischemia-reperfusion injury"@en . . "Dong, J. F." . "Widen, C." . "Wang, X. F." . "Gellert, N." . "[1731634E5502]" . . . . . . "Z(AV0Z50520514), Z(AV0Z50520701)" . "11"^^ . "RIV/68378050:_____/07:00096817" . "148;162" . "Headrick, J. P." . . "RIV/68378050:_____/07:00096817!RIV08-AV0-68378050" . "Dalen, H." . "3" . "1351-0002" . "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 . "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." . . "Witting, P. K." . "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 . . . . "GB - Spojen\u00E9 kr\u00E1lovstv\u00ED Velk\u00E9 Brit\u00E1nie a Severn\u00EDho Irska" . "2"^^ . "Redox Report" . "434067" . "16"^^ . . "Zobalov\u00E1, Renata" . .