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Mitochondria transmit apoptosis signalling in cardiomyocyte-like cells and isolated hearts exposed to experimental ischemia-reperfusion injury
Australien.
Australien.
Australien.
Australien.
Vise andre og tillknytning
2007 (engelsk)Inngår i: Redox report, ISSN 1351-0002, E-ISSN 1743-2928, Vol. 12, nr 3, s. 148-62Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Ischemia-reperfusion (I/R) is a condition leading to serious complications due to death of cardiac myocytes. We used the cardiomyocyte-like cell line H9c2 to study the mechanism underlying cell damage. Exposure of the cells to simulated I/R lead to their apoptosis. Over-expression of Bcl-2 and Bcl-x(L) protected the cells from apoptosis while over-expression of Bax sensitized them to programmed cell death induction. Mitochondria-targeted coenzyme Q (mitoQ) and superoxide dismutase both inhibited accumulation of reactive oxygen species (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.

sted, utgiver, år, opplag, sider
2007. Vol. 12, nr 3, s. 148-62
Emneord [en]
Cardiomyocytes; ischemia/reperfusion; superoxide; apoptosis; mitochondria
HSV kategori
Identifikatorer
URN: urn:nbn:se:hkr:diva-17368DOI: 10.1179/135100007X200227ISI: 000249321000006PubMedID: 17623522OAI: oai:DiVA.org:hkr-17368DiVA, id: diva2:1147727
Tilgjengelig fra: 2017-10-08 Laget: 2017-10-08 Sist oppdatert: 2018-01-13bibliografisk kontrollert

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