CaM Kinase II mediates maladaptive post-infarct remodeling but not acute myocardial ischemia/reperfusion injury

ABSTRACT: Calcium/calmodulin-dependent protein kinase II (CaMKII) was suggested to mediate ischemic myocardial injury and adverse cardiac remodeling. However, the specific functions of the CaMKII isoforms and splice variants in ischemia/reperfusion (I/R) injury have not been investigated yet. Thus, we studied the roles of the CaMKII isoforms and splice variants in I/R by the use of various CaMKII mutant mice. CaMKIIδC was up-regulated already one day after I/R injury but surprisingly, acute I/R injury was neither affected in CaMKIIδ-deficient mice, CaMKIIδ-deficient mice in which the splice variants CaMKIIδB and C were re-expressed nor in conditional CaMKIIδ/γ double-knockout mice (DKO). In contrast, 5 weeks after I/R, DKO mice were protected against extensive scar formation and cardiac dysfun

ORGANISM(S): Mus musculus

SUBMITTER: Carsten Sticht 

PROVIDER: E-GEOD-58486 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress