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

Jun Zhang, Peipei Ping, Guang Wu Wang, Ming Lu, Dawn Pantaleon, Xian Liang Tang, Roberto Bolli, Thomas M. Vondriska

Research output: Contribution to journalArticle

Abstract

Previous studies have indicated that PKC-ε is a central regulator of protective signal transduction in the heart. However, the signaling modules through which PKC-ε exerts its protective effects have only begun to be understood. We have identified a novel participant in the PKC-ε signaling system in cardioprotection, the nonreceptor tyrosine kinase Bmx. Functional proteomic analyses of PKC-e 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.

Original languageEnglish (US)
Pages (from-to)H2364-H2366
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume287
Issue number5 56-5
DOIs
StatePublished - Nov 1 2004

Keywords

  • Myocardial ischemia
  • Nitric oxide
  • Preconditioning
  • Signaling complex
  • Signaling module

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

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