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Maternal hypoxia alternated expression of cardiac proteome and postischemic recovery in adult offspring rats
Author(s) -
Xu Yi,
Armstrong Stephen J.,
Williams Sarah J.,
Davidge Sandra T.
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a757-d
Subject(s) - offspring , medicine , endocrinology , cardiac function curve , intrauterine growth restriction , biology , cardiomyopathy , hypoxia (environmental) , mitochondrion , pregnancy , andrology , gestation , heart failure , chemistry , biochemistry , genetics , organic chemistry , oxygen
Background Intrauterine growth restriction (IUGR) resulting from maternal hypoxia or nutrient restriction during late gestation increases the risk of developing cardiovascular disease in adult offspring. However, the underlying mechanisms that impair later cardiovascular function are unclear. Hypothesis The objective of this study was to identify the cardiac proteome that undergo changes in the isolated heart after aerobic perfusion, or during global ischemia and reperfusion (I/R) from adult offspring by IUGR. Methods Sprague‐Dawley rats were randomized on day 15 of pregnancy to either Hypoxia (IUGR‐H) or Control groups. Female offspring were aged to 7 months at which time hearts were assessed for cardiac function or recovery after I/R. Results A 32 kDa protein was increased while proteins at 50, 86, 226 kDa were decreased in IUGR‐H rats compared to control animals. The proteins were identified as tropomyosin alpha (Tmα), F1F0‐proton ATPase, mitochondrial aconitase, myosin heavy alpha chain (αMHC) using 2D gel electrophoresis and mass spectrometry. In IUGR‐H rats, this remarkably induced cardiac hypertrophy and impaired diastolic function and function recovery after I/R compared to control rats. Furthermore, mitochondrial F1F0‐proton ATPase and mitochondrial aconitase were decreased in IUGR‐H hearts following I/R. Conclusions These findings suggest that maternal hypoxia decreased heart tolerance to I/R, which is associated with the decreased expression of cardiac mitochondria F1F0‐proton ATPase, aconitase and αMHC as well as the increased Tmα in adult offspring rats.