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Does ischemic preconditioning trigger translocation of protein kinase C in the canine model?

Authors: K Przyklenk|||M A Sussman|||B Z Simkhovich|||R A Kloner

Journal: Circulation

Publication Type: Journal Article

Date: 1995

DOI: 10.1161/01.cir.92.6.1546

ID: 7664439

Affiliations:

Affiliations

    Heart Institute, Hospital of the Good Samaritan, Los Angeles, CA 90017, USA.|||||||||

Abstract

Brief episodes of ischemia protect or "precondition" the heart and reduce the size of infarcts caused by subsequent sustained coronary artery occlusion, yet the mechanisms responsible for this cardioprotection remain unresolved. We tested the theory that translocation of protein kinase C (PKC) to the myocyte membranes, initiated in response to brief preconditioning ischemia and manifest during the initial minutes of the sustained occlusion, mediates this phenomenon by attempting to (1) blunt the cardioprotective effects of preconditioning by administration of the PKC inhibitors H-7 and polymyxin B, (2) visualize by fluorescence staining and confocal microscopy changes in the amount or location of PKC, and (3) quantify by incorporation of 32P into PKC-specific peptide changes in the subcellular distribution of PKC in preconditioned versus control hearts.


Chemical List

    Isoquinolines|||Piperazines|||1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine|||Protein Kinase C|||Tetradecanoylphorbol Acetate