Calcium-calmodulin dependent protein kinase II (CaMKII): A main signal responsible for early reperfusion arrhythmias.

100. SAID M, BECERRA R, VALVERDE CA, KAETZEL MA, DEDMAN JR, MUNDIÑA-WEILENMANN C, WEHRENS XH, VITTONE L, MATTIAZZI A.

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY

ACADEMIC PRESS LTD-ELSEVIER SCIENCE LTD

Lugar: Amsterdam; Año: 2011 vol. 51 p. 936 - 944

0022-2828

We explored whether CaMKII-dependent phosphorylation mediate reperfusion arrhythmias in transgenic mice hearts. Results in SR-AIP mice, (CaMKII inhibition of SR proteins and L type Ca2+ channels), indicated a critical role of CaMKII-dependent phosphorylation of these proteins in reperfusion arrhythmias. The experiments in  RyR2-S2814A further indicate that up to 60% of premature beats (PBs) related to CaMKII are dependent on the phosphorylation of RyR2-Ser2814 site and could be ascribed to delayed-afterdepolarizations.  Moreover, phosphorylation of PLN-Thr17 and L-type Ca2+ channels might contribute to reperfusion-induced PBs, by increasing SR Ca2+ content  and Ca2+ influx.