| Autor: |
Tibenska, Veronika, Marvanova, Aneta, Elsnicova, Barbara, Hejnova, Lucie, Vebr, Pavel, Novotný, Jiri, Kolar, Frantisek, Novakova, Olga, Zurmanova, Jitka M. |
| Předmět: |
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| Zdroj: |
Journal of Applied Physiology; Mar2021, Vol. 130 Issue 3, p746-755, 10p |
| Abstrakt: |
The infarct size-limiting effect elicited by cold acclimation (CA) is accompanied by increased mitochondrial resistance and unaltered b1-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 b2-AR/Gi/Akt pathway. Male Wistar rats were exposed to CA (8°C, 5 wk), whereas the recovery group (CAR) was kept at 24°C for additional 2 wk. We show that the total number of myocardial b-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 b2-AR inhibitor ICI-118551 abolished the protective effect in the CAR group but had no effect in the control and CA groups. The inhibitory Gia1/2 and Gia3 proteins increased in the membrane fraction of the CAR group, and the phospho-Akt (Ser473)-to-Akt ratio also increased. Expression, phosphorylation, and mitochondrial location of the Akt target glycogen synthase kinase (GSK-3b) were affected neither by CA nor by CAR. However, GSK-3b 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 b2-AR/Gi 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. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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