Antioxidant tempol suppresses heart cytosolic phospholipase A(2)alpha stimulated by chronic intermittent hypoxia
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F17%3A00477749" target="_blank" >RIV/67985823:_____/17:00477749 - isvavai.cz</a>
Nalezeny alternativní kódy
RIV/00216208:11310/17:10368553 RIV/00216208:11110/17:10368553
Výsledek na webu
<a href="http://dx.doi.org/10.1139/cjpp-2017-0022" target="_blank" >http://dx.doi.org/10.1139/cjpp-2017-0022</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1139/cjpp-2017-0022" target="_blank" >10.1139/cjpp-2017-0022</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
Antioxidant tempol suppresses heart cytosolic phospholipase A(2)alpha stimulated by chronic intermittent hypoxia
Popis výsledku v původním jazyce
Adaptation to chronic intermittent hypoxia (CIH) is associated with reactive oxygen species (ROS) generation implicated in the improved cardiac tolerance against acute ischemia-reperfusion injury. Phospholipases A2 (PLA2s) play an important role in cardiomyocyte phospholipid metabolism influencing membrane homeostasis. Here we aimed to determine the effect of CIH (7000 m, 8 h/day, 5 weeks) on the expression of cytosolic PLA(2) (cPLA(2)alpha), its phosphorylated form (p-cPLA(2)alpha), calcium-independent (iPLA2), and secretory (sPLA2IIA) at protein and mRNA levels, as well as fatty acids (FA) profile in left ventricular myocardium of adult male Wistar rats. Chronic administration of antioxidant tempol was used to verify the ROS involvement in CIH effect on PLA2s expression and phospholipid FA remodeling. While CIH did not affect PLA2s mRNA levels, it increased the total cPLA(2)alpha protein in cytosol and membranes (by 191% and 38%, respectively) and p-cPLA(2)alpha (by 23%) in membranes. Onthe contrary, both iPLA2 and sPLA2IIA were downregulated by CIH. CIH further decreased phospholipid n-6 polyunsaturated FA (PUFA) and increased n-3 PUFA proportion. Tempol treatment prevented only CIH-induced cPLA(2)alpha up-regulation and its phosphorylation on Ser505. Our results show that CIH diversely affect myocardial PLA2s and suggest that ROS are responsible for the activation of cPLA(2)alpha under these conditions.
Název v anglickém jazyce
Antioxidant tempol suppresses heart cytosolic phospholipase A(2)alpha stimulated by chronic intermittent hypoxia
Popis výsledku anglicky
Adaptation to chronic intermittent hypoxia (CIH) is associated with reactive oxygen species (ROS) generation implicated in the improved cardiac tolerance against acute ischemia-reperfusion injury. Phospholipases A2 (PLA2s) play an important role in cardiomyocyte phospholipid metabolism influencing membrane homeostasis. Here we aimed to determine the effect of CIH (7000 m, 8 h/day, 5 weeks) on the expression of cytosolic PLA(2) (cPLA(2)alpha), its phosphorylated form (p-cPLA(2)alpha), calcium-independent (iPLA2), and secretory (sPLA2IIA) at protein and mRNA levels, as well as fatty acids (FA) profile in left ventricular myocardium of adult male Wistar rats. Chronic administration of antioxidant tempol was used to verify the ROS involvement in CIH effect on PLA2s expression and phospholipid FA remodeling. While CIH did not affect PLA2s mRNA levels, it increased the total cPLA(2)alpha protein in cytosol and membranes (by 191% and 38%, respectively) and p-cPLA(2)alpha (by 23%) in membranes. Onthe contrary, both iPLA2 and sPLA2IIA were downregulated by CIH. CIH further decreased phospholipid n-6 polyunsaturated FA (PUFA) and increased n-3 PUFA proportion. Tempol treatment prevented only CIH-induced cPLA(2)alpha up-regulation and its phosphorylation on Ser505. Our results show that CIH diversely affect myocardial PLA2s and suggest that ROS are responsible for the activation of cPLA(2)alpha under these conditions.
Klasifikace
Druh
J<sub>imp</sub> - Článek v periodiku v databázi Web of Science
CEP obor
—
OECD FORD obor
10608 - Biochemistry and molecular biology
Návaznosti výsledku
Projekt
Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.
Návaznosti
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)
Ostatní
Rok uplatnění
2017
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Canadian Journal of Physiology and Pharmacology
ISSN
0008-4212
e-ISSN
—
Svazek periodika
95
Číslo periodika v rámci svazku
8
Stát vydavatele periodika
CA - Kanada
Počet stran výsledku
8
Strana od-do
920-927
Kód UT WoS článku
000407430100007
EID výsledku v databázi Scopus
2-s2.0-85027352195