What question did this study set out to answer?

To identify the specific protein kinase C isozyme that mediates hypoxic preconditioning and protects cardiac myocytes from hypoxia-induced cell death.

December 1, 1997Journal of Biological ChemistryOpen Access

A Selective ε-Protein Kinase C Antagonist Inhibits Protection of Cardiac Myocytes from Hypoxia-induced Cell Death

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Authors

MGMary O. GraySan Francisco General Hospital JKJoel S. KarlinerSchreiner University DMDaria Mochly‐RosenHeart Failure & Transplant

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Implication

In vitro study reveals that epsilon-protein kinase C inhibition abolishes hypoxic preconditioning in cardiac myocytes, indicating its essential role in cardioprotection.

Key Points

To identify the specific protein kinase C isozyme that mediates hypoxic preconditioning and protects cardiac myocytes from hypoxia-induced cell death.
Cultured cardiac myocytes were subjected to hypoxic preconditioning or treatment with 4beta-phorbol 12-myristate 13-acetate prior to 9 hours of prolonged hypoxia.
Assayed the activation of protein kinase C isozymes (epsilon, delta, and betaI) by measuring subcellular translocation.
Introduced a selective epsilon-protein kinase C antagonist, the epsilonV1-2 peptide, to determine whether it inhibits cardioprotection.
Hypoxic preconditioning enhanced cardiac myocyte viability after 9 hours of hypoxia by >50% over control.
Preconditioning induced a 2.1-fold increase in epsilon-protein kinase C activation and a 2.8-fold increase in delta-protein kinase C activation, with no increase in betaI-protein kinase C activation.
Treatment with 4beta-phorbol 12-myristate 13-acetate increased cell survival by 34% compared with control, and treatment with epsilonV1-2 peptide completely abolished both hypoxic preconditioning and phorbol ester-mediated protection.

Cite This Study

Gray et al. (1997) studied this question.

synapsesocial.com/papers/6a708f80439bab0cabc33863 https://doi.org/10.1074/jbc.272.49.30945

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Implication

In vitro study reveals that epsilon-protein kinase C inhibition abolishes hypoxic preconditioning in cardiac myocytes, indicating its essential role in cardioprotection.

A Selective ε-Protein Kinase C Antagonist Inhibits Protection of Cardiac Myocytes from Hypoxia-induced Cell Death

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Implication

Key Points

Cite This Study

A Selective ε-Protein Kinase C Antagonist Inhibits Protection of Cardiac Myocytes from Hypoxia-induced Cell Death

Discussion

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Implication

Key Points

Cite This Study

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