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Proteomic alterations of distinct mitochondrial subpopulations in the type 1 diabetic heart: Contribution of protein import dysfunction
Author(s) -
Baseler Walter A.,
Dabkowski Erinne R.,
Thapa Dharendra,
Croston Tara L.,
Williamson Courtney L.,
Hollander John M.
Publication year - 2011
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.25.1_supplement.825.6
Mitochondrial dysfunction is suggested as an underlying contributor to diabetic cardiomyopathy. Cardiac mitochondria are characterized by subcellular spatial locale including mitochondria located beneath the sarcolemma (SSM), and mitochondria situated between the myofibrils (IFM). The goal of this study was to determine whether diabetic insult influences cardiac proteomic make‐up of spatially‐distinct mitochondrial subpopulations and to evaluate the role of nuclear‐encoded mitochondrial protein import. Utilizing multiple approaches, IFM proteomic make‐up was impacted by diabetic insult to a greater extent than SSM as evidenced by decreased abundance of fatty acid oxidation and electron transport chain proteins. Mitochondrial phosphate carrier, adenine nucleotide translocator, and mitofilin were decreased in the diabetic IFM (p<0.05). Mitochondrial heat shock protein 70 (mtHsp70) was decreased in diabetic IFM (p<0.05). Mitochondrial protein import was decreased in the diabetic IFM (p<0.05). These results indicate that mitochondrial proteomic alterations in the diabetic heart are more pronounced in the IFM. Further, proteomic alterations are associated with nuclear‐encoded mitochondrial protein import dysfunction, implicating this process in the pathogenesis of the diabetic heart. (Supported by NIH DP2DK083095, AHA 0855484D, NIH T32HL090610, AHA 10PRE3420006, AHA 815406D)