ArticleCirculation journal : official journal of the Japanese Circulation Society2012
Identification of εPKC targets during cardiac ischemic injury.
Article in Circulation journal : official journal of the Japanese Circulation Society, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 31 citations in OpenAlex.
- State-Dependent DNA Methylation Signatures Distinguish Acute from Stable Coronary Syndromes.International journal of molecular sciences · 2026Article
- Mitochondrial Fusion, Fission, and Mitophagy in Cardiac Diseases: Challenges and Therapeutic Opportunities.Antioxidants & redox signaling · 2022Review
- Metabolic Remodeling and Implicated Calcium and Signal Transduction Pathways in the Pathogenesis of Heart Failure.International journal of molecular sciences · 2021Review
- Review
- Mitochondrial Bioenergetics and Quality Control Mechanisms in Health and Disease.Oxidative medicine and cellular longevity · 2019Article
- Targeting mitochondrial dysfunction and oxidative stress in heart failure: Challenges and opportunities.Free radical biology & medicine · 2018Review
- PKCε contributes to lipid-induced insulin resistance through cross talk with p70S6K and through previously unknown regulators of insulin signaling.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Cardioprotection induced by a brief exposure to acetaldehyde: role of aldehyde dehydrogenase 2.Cardiovascular research · 2018Article
- Ethanol-Induced Changes in PKCε: From Cell to Behavior.Frontiers in neuroscience · 2018Review
- Cardioprotective Regimen of Adaptation to Chronic Hypoxia Diversely Alters Myocardial Gene Expression in SHR and SHR-mtFrontiers in endocrinology · 2018Article
- Flow-Responsive Vascular Endothelial Growth Factor Receptor-Protein Kinase C Isoform Epsilon Signaling Mediates Glycolytic Metabolites for Vascular Repair.Antioxidants & redox signaling · 2018Article
- Review
- Mitochondrial reactive oxygen species at the heart of the matter: new therapeutic approaches for cardiovascular diseases.Circulation research · 2015Review
- ARF1-regulated coatomer directs the steady-state localization of protein kinase C epsilon at the Golgi apparatus.Biochimica et biophysica acta · 2013Article
- Functional decorations: post-translational modifications and heart disease delineated by targeted proteomics.Genome medicine · 2013Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
Abstract
backgroundEpsilon-protein kinase C (εPKC) protects the heart from ischemic injury. However, the mechanism(s) of εPKC cardioprotection is still unclear. Identification of the εPKC targets may aid in elucidating the εPKC-mediated cardioprotective mechanisms. Previous studies, using εPKC transgenic mice and difference in gel electrophoresis, identified proteins involved in glucose metabolism, the expression of which was modified by εPKC. Those studies were accompanied by metabolomic analysis, suggesting that increased glucose oxidation may be responsible for the cardioprotective effect of εPKC. Whether these εPKC-mediated alterations were because of differences in protein expression or phosphorylation was not determined. METHODS AND
resultsIn the present study, we used an εPKC -specific activator peptide, ψεRACK, combined with phosphoproteomics, to find εPKC targets, and identified that the proteins whose phosphorylation was altered by selective activation of εPKC were mostly mitochondrial proteins. Analysis of the mitochondrial phosphoproteome led to the identification of 55 spots, corresponding to 37 individual proteins, exclusively phosphorylated, in the presence of ψεRACK. The majority of the proteins identified were involved in glucose and lipid metabolism, components of the respiratory chain as well as mitochondrial heat shock proteins.
conclusionsThe protective effect of εPKC during ischemia involves phosphorylation of several mitochondrial proteins involved in glucose and lipid metabolism and oxidative phosphorylation. Regulation of these metabolic pathways by εPKC phosphorylation may lead to εPKC-mediated cardioprotection induced by ψεRACK.
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