Počet záznamů: 1
The cardioprotective effect persisting during recovery from cold acclimation is mediated by the beta(2)-adrenoceptor pathway and Akt activation
- 1.
SYSNO ASEP 0542131 Druh ASEP J - Článek v odborném periodiku Zařazení RIV J - Článek v odborném periodiku Poddruh J Článek ve WOS Název The cardioprotective effect persisting during recovery from cold acclimation is mediated by the beta(2)-adrenoceptor pathway and Akt activation Tvůrce(i) 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)Zdroj.dok. Journal of Applied Physiology. - : American Physiological Society - ISSN 8750-7587
Roč. 130, č. 3 (2021), s. 746-755Poč.str. 10 s. Jazyk dok. eng - angličtina Země vyd. US - Spojené státy americké Klíč. slova beta2-adrenergic signaling ; cardioprotection ; cold acclimation ; glycogen synthase kinase-3beta ; protein kinase B/Akt Vědní obor RIV ED - Fyziologie Obor OECD Physiology (including cytology) CEP GA17-07748S GA ČR - Grantová agentura ČR Způsob publikování Open access Institucionální podpora FGU-C - RVO:67985823 UT WOS 000630429900019 EID SCOPUS 85103227946 DOI 10.1152/japplphysiol.00756.2020 Anotace 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. Pracoviště Fyziologický ústav Kontakt Lucie Trajhanová, lucie.trajhanova@fgu.cas.cz, Tel.: 241 062 400 Rok sběru 2022 Elektronická adresa https://doi.org/10.1152/japplphysiol.00756.2020
Počet záznamů: 1