Počet záznamů: 1  

The cardioprotective effect persisting during recovery from cold acclimation is mediated by the beta(2)-adrenoceptor pathway and Akt activation

  1. 1.
    SYSNO ASEP0542131
    Druh ASEPJ - Článek v odborném periodiku
    Zařazení RIVJ - Článek v odborném periodiku
    Poddruh JČlánek ve WOS
    NázevThe 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. 746-755
    Poč.str.10 s.
    Jazyk dok.eng - angličtina
    Země vyd.US - Spojené státy americké
    Klíč. slovabeta2-adrenergic signaling ; cardioprotection ; cold acclimation ; glycogen synthase kinase-3beta ; protein kinase B/Akt
    Vědní obor RIVED - Fyziologie
    Obor OECDPhysiology (including cytology)
    CEPGA17-07748S GA ČR - Grantová agentura ČR
    Způsob publikováníOpen access
    Institucionální podporaFGU-C - RVO:67985823
    UT WOS000630429900019
    EID SCOPUS85103227946
    DOI10.1152/japplphysiol.00756.2020
    AnotaceThe 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.
    PracovištěFyziologický ústav
    KontaktLucie Trajhanová, lucie.trajhanova@fgu.cas.cz, Tel.: 241 062 400
    Rok sběru2022
    Elektronická adresahttps://doi.org/10.1152/japplphysiol.00756.2020
Počet záznamů: 1  

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