Involvement of PKCepsilon in cardioprotection induced by adaptation to chronic continuous hypoxia
Language English Country Czech Republic Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
25317680
DOI
10.33549/physiolres.932860
PII: 932860
Knihovny.cz E-resources
- MeSH
- Adaptation, Physiological genetics MeSH
- Hypoxia enzymology genetics physiopathology MeSH
- Protein Kinase Inhibitors pharmacology MeSH
- Myocytes, Cardiac drug effects metabolism MeSH
- Rats MeSH
- L-Lactate Dehydrogenase metabolism MeSH
- RNA, Messenger biosynthesis genetics MeSH
- Rats, Wistar MeSH
- Protein Kinase C-epsilon antagonists & inhibitors biosynthesis genetics MeSH
- Myocardial Reperfusion Injury enzymology genetics MeSH
- Cell Survival drug effects MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Protein Kinase Inhibitors MeSH
- L-Lactate Dehydrogenase MeSH
- RNA, Messenger MeSH
- Prkce protein, rat MeSH Browser
- Protein Kinase C-epsilon MeSH
Continuous normobaric hypoxia (CNH) renders the heart more tolerant to acute ischemia/reperfusion injury. Protein kinase C (PKC) is an important component of the protective signaling pathway, but the contribution of individual PKC isoforms under different hypoxic conditions is poorly understood. The aim of this study was to analyze the expression of PKCepsilon after the adaptation to CNH and to clarify its role in increased cardiac ischemic tolerance with the use of PKCepsilon inhibitory peptide KP-1633. Adult male Wistar rats were exposed to CNH (10 % O(2), 3 weeks) or kept under normoxic conditions. The protein level of PKCepsilon and its phosphorylated form was analyzed by Western blot in homogenate, cytosolic and particulate fractions; the expression of PKCepsilon mRNA was measured by RT-PCR. The effect of KP-1633 on cell viability and lactate dehydrogenase (LDH) release was analyzed after 25-min metabolic inhibition followed by 30-min re-energization in freshly isolated left ventricular myocytes. Adaptation to CNH increased myocardial PKCepsilon at protein and mRNA levels. The application of KP-1633 blunted the hypoxia-induced salutary effects on cell viability and LDH release, while control peptide KP-1723 had no effect. This study indicates that PKCepsilon is involved in the cardioprotective mechanism induced by CNH.
References provided by Crossref.org
Unveiling the proteome of the fasting heart: Insights into HIF-1 pathway regulation
Myocardial m6A regulators in postnatal development: effect of sex
The involvement of protein kinases in the cardioprotective effect of chronic hypoxia
