Therapeutic Role of Caveolin‐3 in Mitochondrial Directed Cardioprotection during the Development of Diabetic Cardiomyopathy

Abstract only Diabetes is a worldwide epidemic with cardiovascular disease being a major complication. Caveolins act as scaffolding molecules for regulating signaling. Overexpression of caveolin protects the heart from cardiovascular stress. We hypothesize that cardiac‐specific caveolin‐3 (Cav‐3) ov...

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Bibliographic Details
Published in:	The FASEB journal Vol. 27; no. S1
Main Authors:	Migita, Michael Yoshimichi, Zemljic‐Harpf, Alice E., Finley, J. Cameron, Kellerhals, Sarah E., Fridolfsson, Heidi N., Panneerselvam, Mathivadhani, Niesman, Ingrid R., Ali, Sameh S., Roth, David M., Patel, Hemal H.
Format:	Journal Article
Language:	English
Published:	01-04-2013
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Summary:	Abstract only Diabetes is a worldwide epidemic with cardiovascular disease being a major complication. Caveolins act as scaffolding molecules for regulating signaling. Overexpression of caveolin protects the heart from cardiovascular stress. We hypothesize that cardiac‐specific caveolin‐3 (Cav‐3) overexpression (OE) will protect the diabetic heart. Transgene negative (TGneg) or Cav‐3 OE mice were given a single dose of streptozotocin (75mg/kg) and then placed on a high fat diet to induce type II diabetes mellitus (T2DM). After 3 months, TGneg T2DM mice and Cav‐3 OE T2DM mice showed an increase in body weight, altered glucose tolerance response, and increased insulin levels compared to controls on normal diet. Cav‐3 OE T2DM mitochondria showed protection from calcium swelling and reactive oxygen species generation similar to controls, when compared to TGneg T2DM mitochondria. Cav‐3 OE controls and Cav‐3OE T2DM showed increased protein expression of OPA‐1 and Mitofusin 2, compared to TGneg controls and TGneg T2DM. Mitochondrial ultrastructure (i.e., mitochondrial swelling and clustering) was preserved in Cav‐3 OE T2DM hearts compared to TGneg T2DM. Our data suggest that Cav‐3 OE in the heart has the ability to limit injury in the setting of diabetes through regulation of mitochondrial structure and function.
ISSN:	0892-6638 1530-6860
DOI:	10.1096/fasebj.27.1_supplement.1183.8