Gradual cold acclimation induces cardioprotection without affecting adrenergic beta-receptor-mediated adenylyl cyclase signaling

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F20%3A00524244" target="_blank" >RIV/67985823:_____/20:00524244 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00216208:11310/20:10413518

Výsledek na webu

<a href="https://doi.org/10.1152/japplphysiol.00511.2019" target="_blank" >https://doi.org/10.1152/japplphysiol.00511.2019</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1152/japplphysiol.00511.2019" target="_blank" >10.1152/japplphysiol.00511.2019</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Gradual cold acclimation induces cardioprotection without affecting adrenergic beta-receptor-mediated adenylyl cyclase signaling

Popis výsledku v původním jazyce

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 (beta-AR)-adenylyl cyclase-mediated signaling. Male Wistar rats were exposed to CA (8 degrees C, 8 h/day for a week, followed by 4 wk at 8 degrees C for 24 h/day), while the recovery group (CAR) was kept at 24 degrees 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 mu M Ca2+ was decreased in both groups. Acute administration of metoprolol decreased infarction in control group and did not affect the CA-elicited cardiprotection. Accordingly, neither beta 1-AR-G(s)alpha-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 beta 2- and beta 3-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 beta 2/beta 3-AR pathways remains to be elucidated.

Název v anglickém jazyce

Gradual cold acclimation induces cardioprotection without affecting adrenergic beta-receptor-mediated adenylyl cyclase signaling

Popis výsledku anglicky

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 (beta-AR)-adenylyl cyclase-mediated signaling. Male Wistar rats were exposed to CA (8 degrees C, 8 h/day for a week, followed by 4 wk at 8 degrees C for 24 h/day), while the recovery group (CAR) was kept at 24 degrees 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 mu M Ca2+ was decreased in both groups. Acute administration of metoprolol decreased infarction in control group and did not affect the CA-elicited cardiprotection. Accordingly, neither beta 1-AR-G(s)alpha-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 beta 2- and beta 3-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 beta 2/beta 3-AR pathways remains to be elucidated.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30105 - Physiology (including cytology)

Projekt

<a href="/cs/project/GA17-07748S" target="_blank" >GA17-07748S: Kardioprotektivní potenciál chladové adaptace u potkanů: úloha odpřahujících proteinů.</a><br>

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2020

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Journal of Applied Physiology

ISSN

8750-7587

e-ISSN

—

Svazek periodika

128

Číslo periodika v rámci svazku

4

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

10

Strana od-do

1023-1032

Kód UT WoS článku

000528322200031

EID výsledku v databázi Scopus

2-s2.0-85083545249