Gradual cold acclimation induces cardioprotection without affecting adrenergic β-receptor-mediated adenylyl cyclase signaling
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11310%2F20%3A10413518" target="_blank" >RIV/00216208:11310/20:10413518 - isvavai.cz</a>
Result on the web
<a href="https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=SEx_YpqKvY" target="_blank" >https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=SEx_YpqKvY</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1152/japplphysiol.00511.2019" target="_blank" >10.1152/japplphysiol.00511.2019</a>
Alternative languages
Result language
angličtina
Original language name
Gradual cold acclimation induces cardioprotection without affecting adrenergic β-receptor-mediated adenylyl cyclase signaling
Original language description
Novel strategies are needed that can stimulate endogenous signaling pathways to protect the heart from myocardial infarction. The present study tested the hypothesis that appropriate regimen of cold acclimation (CA) may provide a promising approach for improving myocardial resistance to ischemia/reperfusion (UR) injury without negative side effects. We evaluated myocardial UR injury, mitochondrial swelling, and beta-adrenergic receptor (β-AR)-adenylyl cyclase-mediated signaling. Male Wistar rats were exposed to CA (8 °C, 8 h/day for a week, followed by 4 wk at 8 °C for 24 h/day), while the recovery group (CAR) was kept at 24 °C for an additional 2 wk. The myocardial infarction induced by coronary occlusion for 20 min followed by 3-h reperfusion was reduced from 56% in controls to 30% and 23% after CA and CAR. respectively. In line, the rate of mitochondrial swelling at 200 μM Ca(2+) was decreased in both groups. Acute administration of metoprolol decreased infarction in control group and did not affect the CA-elicited cardiprotection. Accordingly, neither β1-AR-G(s)α-adenyly-1- cyclase signaling. stimulated with specific ligands, nor p-PKA/PICA ratios were affected after CA or CAR. Importantly. Western blot and immunofluorescence analyses revealed β2- and β3-AR protein enrichment in membranes in both experimental groups. We conclude that gradual cold acclimation results in a persisting increase of myocardial resistance to I/R injury without hypertension and hypertrophy. The cardioprotective phenotype is associated with unaltered adenylyl cyclase signaling and increased mitochondrial resistance to Ca2+-overload. The potential role of upregulated β2/β3-AR pathways remains to be elucidated.NEW & NOTEWORTHY: We present a new model of mild gradual cold acclimation increasing tolerance to myocardial ischemia/reperfusion injury without hypertension and hypertrophy. Cardioprotective phenotype is accompanied by unaltered adenylyl cyclase signaling and increased mitochondrial resistance to Ca(2+)-overload. The potential role of upregulated β2/β3-adrenoreceptor activation is considered. These findings may stimulate the development of novel preventive and therapeutic strategies against myocardial ischemia/reperfusion injury.
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
<a href="/en/project/GA17-07748S" target="_blank" >GA17-07748S: Cardioprotective potential of cold acclimation in rats: the role of uncoupling proteins.</a><br>
Continuities
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)
Others
Publication year
2020
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
128
Issue of the periodical within the volume
4
Country of publishing house
US - UNITED STATES
Number of pages
10
Pages from-to
1023-1032
UT code for WoS article
000528322200031
EID of the result in the Scopus database
2-s2.0-85083545249