Involvement of PKCε in cardioprotection induced by adaptation to chronic continuous hypoxia

Title:

Involvement of PKCε in cardioprotection induced by adaptation to chronic continuous hypoxia

Creator:

Holzerová, K., Hlaváčková, M., Jitka Žurmanová, Gudrun Borchert, Jan Neckář, Kolář, F., Novák, F., and Nováková, O.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:60d36ed2-b179-4ff8-bdff-69ad0cfec7e1
uuid:60d36ed2-b179-4ff8-bdff-69ad0cfec7e1
issn:0862-8408

Subject:

Fyziologie člověka a srovnávací fyziologie, hypoxie, proteinové kinázy, hypoxia, protein kinases, chronic hypoxia, cardioprotection, ventricular myocytes, protein kinase C, PKCε inhibitory peptide KP-1633, 14, and 612

Type:

article, články, model:article, and TEXT

Format:

print, bez média, and svazek

Description:

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 PKCε after the adaptation to CNH and to clarify its role in increased cardiac ischemic tolerance with the use of PKCε inhibitory peptide KP-1633. Adult male Wistar rats were exposed to CNH (10 % O2, 3 weeks) or kept under normoxic conditions. The protein level of PKCε and its phosphorylated form was analyzed by Western blot in homogenate, cytosolic and particulate fractions; the expression of PKCε 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 reenergization in freshly isolated left ventricular myocytes. Adaptation to CNH increased myocardial PKCε at protein and mRNA levels. The application of KP-1633 blunted the hypoxiainduced salutary effects on cell viability and LDH release, while control peptide KP-1723 had no effect. This study indicates that PKCε is involved in the cardioprotective mechanism induced by CNH., K. Holzerová, M. Hlaváčková, J. Žurmanová, G. Borchert, J. Neckář, F. Kolář, F. Novák, O. Nováková., and Obsahuje bibliografii

Language:

English

Rights:

http://creativecommons.org/licenses/by-nc-sa/4.0/
policy:public

Source:

Physiological research | 2015 Volume:64 | Number:2

Harvested from:

CDK

Metadata only:

false