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    Fetal Programming and Sexual Dimorphism of Mitochondrial Protein Expression and Activity of Hearts of Prenatally Hypoxic Guinea Pig Offspring

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    Author
    Thompson, L.P.
    Song, H.
    Polster, B.M.
    Date
    2019
    Journal
    Oxidative medicine and cellular longevity
    Publisher
    Hindawi
    Type
    article
    
    Metadata
    Show full item record
    See at
    https://doi.org/10.1155/2019/7210249
    Abstract
    Chronic intrauterine hypoxia is a programming stimulus of cardiovascular dysfunction. While the fetal heart adapts to the reduced oxygenation, the offspring heart becomes vulnerable to subsequent metabolic challenges as an adult. Cardiac mitochondria are key organelles responsible for an efficient energy supply but are subject to damage under hypoxic conditions. We propose that intrauterine hypoxia alters mitochondrial function as an underlying programming mechanism of contractile dysfunction in the offspring. Indices of mitochondrial function such as mitochondrial DNA content, Complex (C) I-V expression, and CI/CIV enzyme activity were measured in hearts of male and female offspring at 90 days old exposed to prenatal hypoxia (10.5% O2) for 14 d prior to term (65 d). Both left ventricular tissue and cardiomyocytes exhibited decreased mitochondrial DNA content, expression of CIV, and CI/CIV activity in male hearts. In female cardiomyocytes, hypoxia had no effect on protein expression of CI-CV nor on CI/CIV activity. This study suggests that chronic intrauterine hypoxia alters the intrinsic properties of select respiratory complexes as a programming mechanism of cardiac dysfunction in the offspring. Sex differences in mitochondrial function may underlie the increased vulnerability of age-matched males compared to females in cardiovascular disease and heart failure.
    Keyword
    chronic intrauterine hypoxia
    cardiovascular dysfunction
    cardiac mitochondria
    Identifier to cite or link to this item
    https://www.scopus.com/inward/record.uri?eid=2-s2.0-85068978199&doi=10.1155%2f2019%2f7210249&partnerID=40&md5=858c88594959aa39d3f05ac0125cc520; http://hdl.handle.net/10713/10213
    ae974a485f413a2113503eed53cd6c53
    10.1155/2019/7210249
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