Ischemic preconditioning induces selective translocation of protein kinase C isoforms ε and η in the heart of conscious rabbits without subcellular redistribution of total protein kinase C activity

Peipei Ping, Jun Zhang, Yumin Qiu, Xian Liang Tang, Srinivas Manchikatapudi, Xinan Cao, Roberto Bolli

Research output: Contribution to journalArticle

Abstract

Considerable controversy surrounds the role of protein kinase C (PKC) in ischemic preconditioning (PC). Previous studies have used pharmacological agents and/or measured total myocardial PKC activity; however, no information is available regarding the effects of PC on individual isoforms in vive. We performed a comprehensive evaluation (using Western immunoblotting) of the expression and subcellular distribution of all 11 currently known PKC isoforms in the heart of conscious rabbits subjected to four different ischemic PC protocols known to induce early and/or late PC (one, three, or six cycles of 4-minute coronary occlusion [4'O]/4-minute reperfusion [4'R]; four cycles of 5-minute occlusion [5'0]/10-minute reperfusion [10'R]). Ten PKC isoforms (α, β12, γ, δ, ε, ζ, η, ι, λ, and μ) were found to be expressed in the rabbit heart. Quantitative immunoblotting demonstrated that as a subgroup, conventional PKCs (cPKCs) are more abundant than novel PKCs (nPKCs) (1445 versus 313 pg PKC/μg tissue protein, respectively) and that PKCα is the predominant isoform among the cPKCs (α, β1, β2, and γ), representing 51% of this subgroup, and PKCε is the most abundant among the nPKCs (δ, ε, ζ, and η), accounting for 62% of this subgroup. None of the ischemic PC protocols examined caused appreciable changes in total PKC activity, in the subcellular distribution of total PKC activity, or in the subcellular distribution of PKC isoforms α, β12, γ, δ, ζ, ι, λ, and μ. In contrast, all PC protocols caused significant translocation of PKCε and PKCη isoforms from the cytosolic to the particulate fraction. The particulate fraction of PKCε increased in a dose-dependent fashion with the number of occlusion/reperfusion cycles performed, from 35±2% in the control group to 43±2% after one 4'O/5-minute reperfusion (5'R) cycle (P

Original languageEnglish (US)
Pages (from-to)404-414
Number of pages11
JournalCirculation Research
Volume81
Issue number3
Publication statusPublished - 1997
Externally publishedYes

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Keywords

  • Late phase of preconditioning
  • Myocardial ischemia
  • Myocardial reperfusion
  • Protein kinase Cε
  • Protein kinase Cη

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

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