onr:"swepub:oai:DiVA.org:liu-49610"
Search: onr:"swepub:oai:DiVA.org:liu-49610" > Mitochondria transm...
- 1 of 1
- Previous record
- Next record
- To hitlist
Mitochondria transmit apoptosis signalling in cardiomyocyte-like cells and isolated hearts exposed to experimental ischemia-reperfusion injury
-
- Neuzil, J. (author)
- Apoptosis Research Group, Heart Foundation Research Centre, Griffith University, Gold Coast Campus, Southport, QLD 9716, Australia, Molecular Therapy Group, Institute of Molecular Genetics, Czech Academy of Sciences, Prague, Czech Republic
-
- Widen, C. (author)
- Widén, C., Apoptosis Research Group, Heart Foundation Research Centre, Griffith University, Gold Coast Campus, Southport, QLD 9716, Australia
-
- Gellert, N. (author)
- Apoptosis Research Group, Heart Foundation Research Centre, Griffith University, Gold Coast Campus, Southport, QLD 9716, Australia
- show more...
- show less...
- Apoptosis Research Group, Heart Foundation Research Centre, Griffith University, Gold Coast Campus, Southport, QLD 9716, Australia, Molecular Therapy Group, Institute of Molecular Genetics, Czech Academy of Sciences, Prague, Czech Republic Widén, C, Apoptosis Research Group, Heart Foundation Research Centre, Griffith University, Gold Coast Campus, Southport, QLD 9716, Australia (creator_code:org_t)
- 2007
- 2007
- English.
- In: Redox report. - 1351-0002 .- 1743-2928. ; 12:3, s. 148-162
- Journal article (peer-reviewed)
Abstract
Subject headings
Close
- 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-xL 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. © W. S. Maney & Son Ltd.
Keyword
- Apoptosis
- Cardiomyocytes
- Ischemia/reperfusion
- Mitochondria
- Superoxide
- MEDICINE
- MEDICIN
Publication and Content Type
- ref (subject category)
- art (subject category)
- 1 of 1
- Previous record
- Next record
- To hitlist
Find more in SwePub
- By the author/editor
- Neuzil, J.
- Widen, C.
- Gellert, N.
- Swettenham, E.
- Zobalova, R.
- Dong, L.-F.
- show more...
- Wang, X.-F.
- Lidebjer, C.
- Dalen, Helge
- Headrick, J.P.
- Witting, P.K.
- show less...
- Articles in the publication
- Redox report
- By the university
- Linköping University
Search outside SwePub
- Extend your search to:
- Google Book Search
- Google Scholar
Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.
- Copyright © LIBRIS - National Library Systems
- LIBRIS.kb.se
