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Bmx, a member of the Tec family of nonreceptor tyrosine kinases, is a novel participant in pharmacological cardioprotection

¹Departments of Physiology and Medicine/Cardiology, Cardiovascular Research Laboratories, David Geffen School of Medicine at University of California Los Angeles, Los Angeles, California 90095; and ²Division of Cardiology, University of Louisville, Louisville, Kentucky 40292

Submitted 10 May 2004 ; accepted in final form 1 June 2004

Previous studies have indicated that PKC- is a central regulator of protective signal transduction in the heart. However, the signaling modules through which PKC- exerts its protective effects have only begun to be understood. We have identified a novel participant in the PKC- signaling system in cardioprotection, the nonreceptor tyrosine kinase Bmx. Functional proteomic analyses of PKC- signaling complexes identified Bmx as a member of these complexes. Subsequent studies in rabbits have indicated that Bmx is activated by nitric oxide (NO) in the heart, concomitant with the late phase of NO donor-induced protection, and provide the first analysis of Bmx expression/distribution in the setting of cardioprotection. In addition, increased expression of Bmx induced by NO donors was blocked by the same mechanism that blocked cardioprotection: inhibition of PKC with chelerythrine. These findings indicate that a novel type of PKC-tyrosine kinase module (involving Bmx) is formed in the heart and may be involved in pharmacological cardioprotection by NO donors.

myocardial ischemia; preconditioning; signaling complex; signaling module; nitric oxide

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