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  • Title: Proteome changes in CaMKIIδC-overexpressing cardiac myocytes.
    Author: Schott P, Jacobshagen C, Köhler J, Seidler T, Asif AR, Dihazi H, Hasenfuss G, Maier LS.
    Journal: Cardiovasc Pathol; 2010; 19(6):e241-50. PubMed ID: 20093047.
    Abstract:
    Recent studies have demonstrated that the expression as well as the activity of Ca/calmodulin-dependent protein kinase IIδ(C) (CaMKIIδ(C)) is increased in heart failure. Transgenic overexpression of CaMKIIδ(C) in mouse hearts results in severe dilated cardiomyopathy. So far, little is known about CaMKIIδ(C)-induced changes in gene expression and proteome alteration. We hypothesize that proteome changes similar to those found in advanced heart failure can be assessed even after short term overexpression of CaMKIIδ(C) in an in vitro culture model. Thus, we designed a study using a proteomic approach combined with adenovirus-mediated gene transfer of CaMKIIδ(C) to identify early CaMKIIδ(C)-induced changes in cardiac myocyte phenotype on proteome level. CaMKIIδ(C) was overexpressed by adenovirus-mediated gene transfer in isolated cardiac myocytes of adult rabbits for 48 h. Proteome changes were analyzed by two-dimensional gel electrophoresis and mass spectrometry (MS). Overexpression of CaMKIIδ(C) resulted in a decreased expression of 21 proteins (at least twofold change of expression, P<.05, n=10). Using in-gel digest and MS, we identified 13 out of these 21 proteins. CaMKIIδ(C) overexpression leads to a reduced abundance of NADH dehydrogenase, lactate dehydrogenase, pyruvate kinase, dihydrolipoamide succinyltransferase, creatine kinase M, heat shock protein 70, elongation factor Tu, and superoxide dismutase. The profile of the proteome changes induced by CaMKIIδ(C) overexpression after 48 h displayed striking alterations of metabolic proteins, cell-protecting proteins including antioxidants, and proteins involved in protein synthesis. Interestingly, the observed proteome changes are in common with the phenotype of failing cardiac myocytes on the protein level. These altered proteins may act individually as contributors to heart failure, which is observed after overexpression of CaMKIIδ(C) in genetically altered mice.
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