Receptor-independent cardiac protein kinase Calpha activation by calpain-mediated truncation of regulatory domains.

ABSTRACT:

Rationale

Protein kinase (PK)Cs and calpain cysteine proteases are highly expressed in myocardium. Ischemia produces calcium overload that activates calpains and conventional PKCs. However, calpains can proteolytically process PKCs, and the potential in vivo consequences of this interaction are unknown.

Objective

To determine the biochemical and pathophysiological consequences of calpain-mediated cardiac PKCα proteolysis.

Methods and results

Isolated mouse hearts subjected to global ischemia/reperfusion demonstrated cleavage of PKCα. Calpain 1 overexpression was not sufficient to produce PKCα cleavage in normal hearts, but ischemia-induced myocardial PKCα cleavage and myocardial injury were greatly increased by cardiac-specific expression of calpain 1. In contrast, ca

SUBMITTER: Kang MY 

PROVIDER: S-EPMC2948630 | biostudies-literature | 2010 Oct

REPOSITORIES: biostudies-literature