Increased Collagen Deposition and Diastolic Dysfunction but Preserved Myocardial Hypertrophy After Pressure Overload in Mice Lacking PKCε

Overexpression and activation of protein kinase C-ε (PKCε) results in myocardial hypertrophy. However, these observations do not establish that PKCε is required for the development of myocardial hypertrophy. Thus, we subjected PKCε-knockout (KO) mice to a hypertrophic stimulus by transverse aortic constriction (TAC). KO mice show normal cardiac morphology and function. TAC caused similar cardiac hypertrophy in KO and wild-type (WT) mice. However, KO mice developed more interstitial fibrosis and showed enhanced expression of collagen Iα1 and collagen III after TAC associated with diastolic dysfunction, as assessed by tissue Doppler echocardiography (Ea/Aa after TACWT 2.1±0.3 versus KO 1.0±0.2; P