Novel Cardiac Apoptotic Pathway

• DOI: 10.1161/circulationaha.107.750869
• Publication Date: 2008-11-11T01:34:32Z
• Authors: Wei-Qi Tan; Jian-Xun Wang; Zhi-Qiang Lin; Yan-Rui Li; Yu Lin; Pei-Feng Li
• Keywords: Dephosphorylation

Background— Apoptosis repressor with caspase recruitment domain (ARC) is abundantly expressed in cardiomyocytes. Protein kinase CK2 can phosphorylate ARC at threonine-149, thereby enabling to antagonize apoptosis. phosphorylation occurs a constitutive manner. Nevertheless, cardiomyocytes still undergo apoptosis that related cardiac diseases such as myocardial infarction and heart failure. Whether the occurrence of loss protection by under pathological conditions remains unknown. Methods Results— levels are decreased treated isoproterenol or aldosterone. We explored molecular mechanism which decreased. Our results reveal either direct incubation coexpression calcineurin leads decrease levels. Inhibition attenuate reduction on treatment These data indicate its dephosphorylation calcineurin. further prevent isoproterenol- aldosterone-induced apoptosis, but this function depends status. Isoproterenol aldosterone upregulate Fas ligand expression, caspase-8 required for induce However, phosphorylated not dephosphorylated able inhibit caspase-8–mediated Phosphorylated exerts effects against directly associating procaspase-8 inhibiting interaction Fas-associated protein death domain. Conclusions— study identifies novel apoptotic pathway This could be component machinery.