Summary
The PKC hypothesis and its variants are attractive but unproved. The chief difficulty is the lack of an objective means to assess whether or not PKC has been activated in hearts preconditionedin vivo with ischemia or in hearts preconditioned by pharmacologic means. The strongest evidence is supporting the PKC hypothesisin vivo is the prevention of preconditioning with antagonists such as staurosporine. However, these data are weakened by the failure of these agents to aliminate PC in large animal hearts. Since hearts of virtually all mammalian species can be preconditioned, it seems likely that the general mechanism causing it is similar in each and should respond to a strong inhibitor. More work needs to be done.
This is a preview of subscription content, log in via an institution to check access.
Similar content being viewed by others
References
Louis JC, Magal E, Vavin E (1986) Protein kinase-C alterations in the fetal rat brain after global ischemia. J Biol Chem 263:19282–19285
Light PE, Sabir AA, Allen BG, Walsh MP, French RJ (1996) Protein kinase-C induced changes in the stoichiometry of ATP-binding activate cardiac ATP-sensitive K+ channels. A possible mechanistic link to ischemic preconditioning. Circ Res 79:399–406
Author information
Authors and Affiliations
Additional information
Supported in part by NIH grants HL 23138 & 27426.
Rights and permissions
About this article
Cite this article
Jennings, R.B. Role of protein kinase C in preconditioning with ischemia against lethal cell injury. Basic Res Cardiol 92 (Suppl 2), 40–42 (1997). https://doi.org/10.1007/BF00797206
Issue Date:
DOI: https://doi.org/10.1007/BF00797206