Chronic intermittent hypoxia affects the cytosolic phospholipase A(2)alpha/cyclooxygenase 2 pathway via beta(2)-adrenoceptor-mediated ERK/p38 stimulation
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F16%3A00466474" target="_blank" >RIV/67985823:_____/16:00466474 - isvavai.cz</a>
Nalezeny alternativní kódy
RIV/00216208:11310/16:10332874
Výsledek na webu
<a href="http://dx.doi.org/10.1007/s11010-016-2833-8" target="_blank" >http://dx.doi.org/10.1007/s11010-016-2833-8</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1007/s11010-016-2833-8" target="_blank" >10.1007/s11010-016-2833-8</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
Chronic intermittent hypoxia affects the cytosolic phospholipase A(2)alpha/cyclooxygenase 2 pathway via beta(2)-adrenoceptor-mediated ERK/p38 stimulation
Popis výsledku v původním jazyce
Cardiac resistance against acute ischemia/reperfusion (I/R) injury can be enhanced by adaptation to chronic intermittent hypoxia (CIH), but the changes at the molecular level associated with this adaptation are still not fully explored. Phospholipase A(2) (PLA(2)) plays an important role in phospholipid metabolism and may contribute to membrane destruction under conditions of energy deprivation during I/R. The aim of this study was to determine the effect of CIH (7000 m, 8 h/day, 5 weeks) on the expression of cytosolic PLA(2)alpha (cPLA(2)alpha) and its phosphorylated form (p-cPLA(2)alpha), as well as other related signaling proteins in the left ventricular myocardium of adult male Wistar rats. Adaptation to CIH increased the total content of cPLA(2)alpha by 14 % in myocardial homogenate, and enhanced the association of p-cPLA(2)alpha with the nuclear membrane by 85 %. The total number of beta-adrenoceptors (beta-ARs) did not change but the beta(2)/beta(1) ratio markedly increased due to the elevation of beta(2)-ARs and drop in beta(1)-ARs. In parallel, the amount of adenylyl cyclase decreased by 49 % and G(i)alpha proteins increased by about 50 %. Besides that, cyclooxygenase 2 (COX-2) and prostaglandin E-2 (PGE(2)) increased by 36 and 84 %, respectively. In parallel, we detected increased phosphorylation of protein kinase C alpha, ERK1/2 and p38 (by 12, 48 and 19 %, respectively). These data suggest that adaptive changes induced in the myocardium by CIH may include activation of cPLA(2)alpha and COX-2 via beta(2)-AR/G(i)-mediated stimulation of the ERK/p38 pathway.
Název v anglickém jazyce
Chronic intermittent hypoxia affects the cytosolic phospholipase A(2)alpha/cyclooxygenase 2 pathway via beta(2)-adrenoceptor-mediated ERK/p38 stimulation
Popis výsledku anglicky
Cardiac resistance against acute ischemia/reperfusion (I/R) injury can be enhanced by adaptation to chronic intermittent hypoxia (CIH), but the changes at the molecular level associated with this adaptation are still not fully explored. Phospholipase A(2) (PLA(2)) plays an important role in phospholipid metabolism and may contribute to membrane destruction under conditions of energy deprivation during I/R. The aim of this study was to determine the effect of CIH (7000 m, 8 h/day, 5 weeks) on the expression of cytosolic PLA(2)alpha (cPLA(2)alpha) and its phosphorylated form (p-cPLA(2)alpha), as well as other related signaling proteins in the left ventricular myocardium of adult male Wistar rats. Adaptation to CIH increased the total content of cPLA(2)alpha by 14 % in myocardial homogenate, and enhanced the association of p-cPLA(2)alpha with the nuclear membrane by 85 %. The total number of beta-adrenoceptors (beta-ARs) did not change but the beta(2)/beta(1) ratio markedly increased due to the elevation of beta(2)-ARs and drop in beta(1)-ARs. In parallel, the amount of adenylyl cyclase decreased by 49 % and G(i)alpha proteins increased by about 50 %. Besides that, cyclooxygenase 2 (COX-2) and prostaglandin E-2 (PGE(2)) increased by 36 and 84 %, respectively. In parallel, we detected increased phosphorylation of protein kinase C alpha, ERK1/2 and p38 (by 12, 48 and 19 %, respectively). These data suggest that adaptive changes induced in the myocardium by CIH may include activation of cPLA(2)alpha and COX-2 via beta(2)-AR/G(i)-mediated stimulation of the ERK/p38 pathway.
Klasifikace
Druh
J<sub>x</sub> - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)
CEP obor
FA - Kardiovaskulární nemoci včetně kardiochirurgie
OECD FORD obor
—
Návaznosti výsledku
Projekt
<a href="/cs/project/GA13-10267S" target="_blank" >GA13-10267S: Ischemická tolerance srdcí spontánně hypertenzních potkanů: význam mitochondriálního genomu</a><br>
Návaznosti
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Ostatní
Rok uplatnění
2016
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Molecular and Cellular Biochemistry
ISSN
0300-8177
e-ISSN
—
Svazek periodika
423
Číslo periodika v rámci svazku
1-2
Stát vydavatele periodika
US - Spojené státy americké
Počet stran výsledku
13
Strana od-do
151-163
Kód UT WoS článku
000387365600015
EID výsledku v databázi Scopus
2-s2.0-84989184220