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ABSTRACT: Background and purpose
Previous studies of ischemia-reperfusion injury (IRI) in hearts from mice with cardiac-restricted overexpression of CCN2 have shown that CCN2 increases tolerance towards IRI. The objectives of this study were to investigate to what extent post-ischemic administration of recombinant human CCN2 (rhCCN2) would limit infarct size and improve functional recovery and what signaling pathways are involved.Experimental approach
Isolated mice hearts were perfused ad modum Langendorff, subjected to no-flow, global ischemia, and subsequently, exposed to mammalian cell derived, full-length (38-40kDa) rhCCN2 (250 nM) or vehicle during the first 15 min of a 60 min reperfusion period.Key results
Post-ischemic administration of rhCCN2 resulted in attenuation o
SUBMITTER: Kaasboll OJ
PROVIDER: S-EPMC4752337 | biostudies-literature | 2016
REPOSITORIES: biostudies-literature