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dc.contributor.author Csonka, Csaba
dc.contributor.author Szűcs, Gergő
dc.contributor.author Varga-Orvos, Zoltán
dc.contributor.author Bencsik, Péter
dc.contributor.author Csont, Tamás Bálint
dc.contributor.author Zvara, Ágnes
dc.contributor.author Puskás, László
dc.contributor.author Ferdinandy, Péter
dc.date.accessioned 2018-08-30T09:32:53Z
dc.date.available 2018-08-30T09:32:53Z
dc.date.issued 2014
dc.identifier 84893931612
dc.identifier.citation pagination=141-150; journalVolume=239; journalIssueNumber=2; journalTitle=EXPERIMENTAL BIOLOGY AND MEDICINE;
dc.identifier.uri http://repo.lib.semmelweis.hu//handle/123456789/6237
dc.identifier.uri doi:10.1177/1535370213511017
dc.description.abstract To profile changes in gene expression in response to ischemic postconditioning, isolated rat hearts were subjected to 30 min of regional ischemia followed by 120 min of reperfusion with or without postconditioning. At the end of reperfusion, cardiac RNA was assayed by DNA microarrays (31,000 format), verified by quantitative real-time polymerase chain reaction (QRT-PCR). Postconditioning significantly up-regulated 50 genes and down-regulated 58 different genes, including pyruvate dehydrogenase, 60 kDa heat shock protein 1, lipoprotein lipase, gamma-sarcoglycan, and phospholipase C. Gene ontology analysis revealed that most of the altered genes belong to the cellular metabolic processes cluster. Many of the genes have not previously been suspected to be involved in the mechanism of postconditioning.
dc.relation.ispartof urn:issn:1535-3702
dc.title Ischemic postconditioning alters the gene expression pattern of the ischemic heart
dc.type Journal Article
dc.date.updated 2018-08-28T20:31:07Z
dc.language.rfc3066 en
dc.identifier.mtmt 2500771
dc.identifier.wos 000331556100002
dc.identifier.pubmed 24414479
dc.contributor.department SE/AOK/I/Farmakológiai és Farmakoterápiás Intézet
dc.contributor.institution Semmelweis Egyetem


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