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Enhanced apoptotic propensity in diabetic cardiac interfibrillar mitochondria
Author(s) -
Williamson Courtney L,
Dabkowski Erinne R,
Hollander John M
Publication year - 2008
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.22.1_supplement.1238.19
Subject(s) - diabetic cardiomyopathy , diabetes mellitus , mitochondrion , apoptosis , cytochrome c , pathogenesis , medicine , endocrinology , streptozotocin , cardiomyopathy , mitochondrial dna , cardiology , microbiology and biotechnology , chemistry , biology , heart failure , biochemistry , gene
Cardiovascular complications, including diabetic cardiomyopathy, are the leading cause of mortality among diabetic patients. Enhanced mitochondrion‐dependent apoptosis is associated with diabetic cardiomyopathy pathogenesis. Two spatially distinct mitochondria populations exist in the cardiac myocyte, interfibrillar mitochondria (IFM), which situate between the contractile apparatus, and subsarcolemmal mitochondria (SSM), which exist beneath the plasma membrane. The goal of this study was to determine the impact of diabetic insult on the apoptotic propensity of spatially distinct mitochondrial populations. Swiss Webster mice were made diabetic by streptozotocin injection and sacrificed following diabetes onset. Our findings indicate that diabetic IFM display a greater propensity for undergoing apoptosis as compared to SSM. Specifically, mitochondrial permeability transition pore time to V max was decreased in diabetic IFM as compared to control ( P <0.05), with no difference in SSM. Mitochondrial membrane potential was decreased in diabetic IFM as compared to control ( P <0.05) with no difference in SSM. Mitochondrial cytochrome C content in IFM was decreased as a result of diabetic insult. These results indicate that cardiac IFM are more susceptible to diabetes‐associated apoptosis, and may be more contributory to the pathogenesis of diabetic cardiomyopathy. (Supported by AHA 0665237B)