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Antioxidant tempol suppresses heart cytosolic phospholipase A(2)alpha stimulated by chronic intermittent hypoxia

The result's identifiers

  • Result code in 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>

  • Alternative codes found

    RIV/00216208:11310/17:10368553 RIV/00216208:11110/17:10368553

  • Result on the web

    <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>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Antioxidant tempol suppresses heart cytosolic phospholipase A(2)alpha stimulated by chronic intermittent hypoxia

  • Original language description

    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.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    10608 - Biochemistry and molecular biology

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

    2017

  • Confidentiality

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

Data specific for result type

  • Name of the periodical

    Canadian Journal of Physiology and Pharmacology

  • ISSN

    0008-4212

  • e-ISSN

  • Volume of the periodical

    95

  • Issue of the periodical within the volume

    8

  • Country of publishing house

    CA - CANADA

  • Number of pages

    8

  • Pages from-to

    920-927

  • UT code for WoS article

    000407430100007

  • EID of the result in the Scopus database

    2-s2.0-85027352195