Abstract
BackgroundThe incidence of MI rises sharply at the time of menopause, implicating loss of estrogen (E2) in age‐related increases in ischemic injury.PurposeTo identify new mitochondrial protein targets for the treatment of acute MI in aged women using a state‐of‐the‐art proteomics approach. We hypothesized that E2 deficiency exacerbates age‐dependent disruptions in mitochondrial proteins in female rat heart.MethodsTargeted proteomic analyses were conducted in mitochondria isolated from left ventricles of adult (6 mo) and aged (24 mo) F344 ovary‐intact or ovariectomized (OVX) rats using the newly released isobaric tags for relative and absolute quantification (iTRAQ) 8plex labeling and mass spectrometry (n=4‐5/group).ResultsInitial multi‐dimensional protein identification technology (MudPIT) analyses revealed n=638 distinct mitochondrial proteins. With iTRAQ, significant group differences (false discovery rate < 5%) were observed in proteins related to cellular metabolism, ion transport, oxidative stress and cell death regulation. Effects of age‐associated E2 deficiency were primarily limited to proteins which regulate oxidative stress, and were not observed in adult OVX.ConclusionsProteomic analysis through iTRAQ is effective in identifying new candidate proteins for further in‐depth study of age‐ and E2‐dependent alterations in mitochondrial cardioprotective signaling.
Published Version
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