Full metadata record
DC Field | Value | Language |
---|---|---|
dc.creator | Beaumont, J. (Javier) | - |
dc.creator | Arias, T. (Teresa) | - |
dc.creator | Ravassa, S. (Susana) | - |
dc.creator | Diez-Martinez, J. (Javier) | - |
dc.date.accessioned | 2012-05-02T07:50:13Z | - |
dc.date.available | 2012-05-02T07:50:13Z | - |
dc.date.issued | 2008 | - |
dc.identifier.citation | Beaumont J, Arias T, Ravassa S, Diez J. Overexpression of human truncated peroxisome proliferator-activated receptor alpha induces apoptosis in HL-1 cardiomyocytes. Cardiovasc Res 2008 Aug 1;79(3):458-463. | es_ES |
dc.identifier.issn | 1755-3245 | - |
dc.identifier.uri | https://hdl.handle.net/10171/21850 | - |
dc.description.abstract | AIMS: Our goal was to analyse whether truncated peroxisome proliferator-activated receptor alpha (PPARalpha) overexpression induces apoptosis of cardiomyocytes. METHODS AND RESULTS: We constructed a recombinant vector of human truncated PPARalpha and a mammalian expression vector to transfect PPARalpha into a line of murine cardiomyocytes designated HL-1. Four hallmarks of apoptosis were measured in these transfected cells: depolarization of mitochondrial membrane, activation of caspase-3, phosphatidylserine (PS) externalization, and DNA fragmentation. Co-transfection with human cyclic adenosine monophosphate response element-binding protein (CREB) and human CREB binding protein (CBP) and analysis of apoptosis regulatory proteins, Bcl-2 and Bax, were also performed in truncated PPARalpha-transfected cells to determine the potential mechanisms by which truncated PPARalpha may influence apoptosis. Progressive depolarization of mitochondrial membrane, activation of caspase-3, PS externalization, DNA fragmentation, and cell death were observed in HL-1 cells upon increasing levels of transfected truncated PPARalpha. The expression of the antiapoptotic protein Bcl-2 decreased in transfected HL-1 cardiomyocytes, whereas no changes in the proapoptotic protein Bax were observed in these cells. Overexpression of CREB plus CBP abolished the inhibitory effect of truncated PPARalpha on Bcl-2 protein. CONCLUSION: These results demonstrate that human truncated PPARalpha overexpression induces apoptosis in HL-1 cardiomyocytes. In addition, our findings suggest that truncated PPARalpha may induce cardiomyocyte apoptosis through the inhibition of the antiapoptotic protein, Bcl-2. It is proposed that competition with CREB for coactivators like CBP could be involved in this inhibitory effect. | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | Oxford University Press | es_ES |
dc.rights | info:eu-repo/semantics/closedAccess | - |
dc.subject | Truncated PPARα | es_ES |
dc.subject | Apoptosis | es_ES |
dc.subject | Cardiomyocytes | es_ES |
dc.title | Overexpression of human truncated peroxisome proliferator-activated receptor alpha induces apoptosis in HL-1 cardiomyocytes | es_ES |
dc.type | info:eu-repo/semantics/article | es_ES |
dc.relation.publisherversion | http://cardiovascres.oxfordjournals.org/content/79/3/458 | es_ES |
dc.type.driver | info:eu-repo/semantics/article | es_ES |
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