Premium
Mitochondrial subpopulation‐specific proteomic alterations in the type 2 diabetic heart
Author(s) -
Croston Tara Lyne,
Dabkowski Erinne R,
Williamson Courtney L,
Baseler Walter A,
Hollander John M
Publication year - 2010
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.24.1_supplement.lb573
Subject(s) - mitochondrion , diabetic cardiomyopathy , medicine , cytochrome c oxidase , endocrinology , coenzyme q – cytochrome c reductase , peroxiredoxin , electron transport chain , cardiomyopathy , diabetes mellitus , protein subunit , type 2 diabetes , cytochrome c , ubiquinol , pathogenesis , inner mitochondrial membrane , biology , microbiology and biotechnology , biochemistry , heart failure , gene , enzyme , peroxidase
Diabetic cardiomyopathy is the leading cause of mortality in patients who suffer from diabetes mellitus (DM). Mitochondria dysfunction contributes to the cardiac complications associated with type 2 DM. Cardiomyocytes contain two spatially distinct mitochondrial subpopulations, interfibrillar mitochondria (IFM) and subsarcolemmal mitochondria (SSM). The goal of this study was to determine whether the proteomic profiles of the two cardiac mitochondrial subpopulations were influenced differently by type 2 diabetic insult. Db/db mice and WT controls were sacrificed at 18 weeks of age and cardiac mitochondrial subpopulations were isolated. Proteomic analysis revealed a decrease in proteins involved in the electron transport chain (ETC) complexes in the SSM. Specifically, ubiquinol cytochrome c reductase core protein 2 (complex III) and cytochrome c oxidase subunit VIIa1 (complex IV) were downregulated in db/db SSM. Further, peroxiredoxin V (PRDX5), an antioxidant, and adenine nucleotide transporter 1 (ANT1), an inner mitochondrial membrane transport protein, were also significantly decreased only in db/db SSM. These results suggest that the SSM are at greater risk for protein loss as a result of type 2 DM, which may contribute to the pathogenesis of diabetic cardiomyopathy. (Supported by NIH DP2 DK083095, AHA0815406D, AHA0855484D)