Effect of cardiomyocyte and vascular smooth muscle cell specific KO of p38 MAPKα on gene expression profile of the heart

p38MAPKα KO mice develop in response to Angiotensin II treatment a dilative cardiomyopathy. Gene expression profile of KO hearts was compared to equally treated control heart under baseline conditions and after 48 hours of Angiotensin II treatment via osmotic mini pumps. Gene expression of mouse hearts of conditional p38 KO mice. Mice express a cre recombinase under control of SM22α promotor and a p38 MAPKα gene, which has loxPside-flanked exons 2 and 3. This expression lead to a specific KO of p38 MAPKα in vascular smooth muscle cells and cardiomyocytes. Control mice only express the floxed p38MAPKα gene. For RNA isolation four hearts of control and KO mice were harvested from untreated 3 month old male mice (Basal) and after 48 hours treatment with Angiotensin II (AngII) (1.5mg/kg/d). RNA was isolated from heart apex.