The cardioprotective effect persisting during recovery from cold acclimation is mediated by the beta(2)-adrenoceptor pathway and Akt activation
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F21%3A00542131" target="_blank" >RIV/67985823:_____/21:00542131 - isvavai.cz</a>
Alternative codes found
RIV/00216208:11310/21:10431528
Result on the web
<a href="https://doi.org/10.1152/japplphysiol.00756.2020" target="_blank" >https://doi.org/10.1152/japplphysiol.00756.2020</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1152/japplphysiol.00756.2020" target="_blank" >10.1152/japplphysiol.00756.2020</a>
Alternative languages
Result language
angličtina
Original language name
The cardioprotective effect persisting during recovery from cold acclimation is mediated by the beta(2)-adrenoceptor pathway and Akt activation
Original language description
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.
Czech name
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Czech description
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Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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OECD FORD branch
30105 - Physiology (including cytology)
Result continuities
Project
Result was created during the realization of more than one project. More information in the Projects tab.
Continuities
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)
Others
Publication year
2021
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Journal of Applied Physiology
ISSN
8750-7587
e-ISSN
1522-1601
Volume of the periodical
130
Issue of the periodical within the volume
3
Country of publishing house
US - UNITED STATES
Number of pages
10
Pages from-to
746-755
UT code for WoS article
000630429900019
EID of the result in the Scopus database
2-s2.0-85103227946