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The cardioprotective effect persisting during recovery from cold acclimation is mediated by the beta(2)-adrenoceptor pathway and Akt activation
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SYSNO ASEP 0542131 Document Type J - Journal Article R&D Document Type Journal Article Subsidiary J Článek ve WOS Title The cardioprotective effect persisting during recovery from cold acclimation is mediated by the beta(2)-adrenoceptor pathway and Akt activation Author(s) Tibenská, V. (CZ)
Marvanová, A. (CZ)
Elsnicová, B. (CZ)
Hejnová, L. (CZ)
Vebr, P. (CZ)
Novotný, J. (CZ)
Kolář, František (FGU-C) RID, ORCID, SAI
Nováková, Olga (FGU-C)
Žurmanová, J.M. (CZ)Source Title Journal of Applied Physiology. - : American Physiological Society - ISSN 8750-7587
Roč. 130, č. 3 (2021), s. 746-755Number of pages 10 s. Language eng - English Country US - United States Keywords beta2-adrenergic signaling ; cardioprotection ; cold acclimation ; glycogen synthase kinase-3beta ; protein kinase B/Akt Subject RIV ED - Physiology OECD category Physiology (including cytology) R&D Projects GA17-07748S GA ČR - Czech Science Foundation (CSF) Method of publishing Open access Institutional support FGU-C - RVO:67985823 UT WOS 000630429900019 EID SCOPUS 85103227946 DOI 10.1152/japplphysiol.00756.2020 Annotation The infarct size-limiting effect elicited by cold acclimation (CA) is accompanied by increased mitochondrial resistance and unaltered beta(1)-adrenergic receptor (AR) signaling persisting for 2 wk at room temperature. As the mechanism of CA-elicited cardioprotection is not fully understood, we examined the role of the salvage beta(2)-AR/G(i)/Akt pathway. Male Wistar rats were exposed to CA (8 degrees C, 5 wk), whereas the recovery group (CAR) was kept at 24 degrees C for additional 2 wk. We show that the total number of myocardial beta-ARs in the left ventricular myocardium did not change after CA but decreased after CAR. We confirmed the infarct size-limiting effect in both CA and CAR groups. Acute administration of beta(2)-AR inhibitor ICI-118551 abolished the protective effect in the CAR group but had no effect in the control and CA groups. The inhibitory G(i)alpha(1/2) and G(i)alpha(3) proteins increased in the membrane fraction of the CAR group, and the phospho-Akt (Ser(473))-to-Akt ratio also increased. Expression, phosphorylation, and mitochondrial location of the Akt target glycogen synthase kinase (GSK-3 beta) were affected neither by CA nor by CAR. However, GSK-3 beta translocated from the Z-disk to the H-zone after CA, and acquired its original location after CAR. Our data indicate that the cardioprotection observed after CAR is mediated by the beta 2-AR/G(i) pathway and Akt activation. Further studies are needed to unravel downstream targets of the central regulators of the CA process and the downstream targets of the Akt protein after CAR. Workplace Institute of Physiology Contact Lucie Trajhanová, lucie.trajhanova@fgu.cas.cz, Tel.: 241 062 400 Year of Publishing 2022 Electronic address https://doi.org/10.1152/japplphysiol.00756.2020
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