Regulation of A-Kinase-Anchoring Protein 12 by Heat Shock Protein A12B to Prevent Ventricular Dysfunction Following Acute Myocardial Infarction in Diabetic Rats.

We examined the effects of overexpressing on angiogenesis and myocardial function by intramyocardial administration of adenovirus encoding Hduanyu184212B (Ad. in a streptozotocin-induced diabetic rat subjected to myocardial infarction. Rats were divided randomly into six groups: control sham (CS) + Ad.LacZ, control myocardial infarction (CMI) + Ad.LacZ, control diabetic sham (DS) + Ad.LacZ, diabetic MI + Ad.LacZ and diabetic Following MI or sham surgery, the respective groups received either Ad.LacZ or via intramyocardial injections. We observed increased capillary and arteriolar density along with reduced fibrosis and preserved heart functions in compared to DMI-AdLacZ group. Western blot analysis demonstrated enhanced vascular endothelial growth factor (VEGF), thioredoxin-1 (Trx-1) expression along with decreased expression of thioredoxin interacting protein (TXNIP) and A kinase anchoring protein 12 (AKAP12) in the DMI-AdHduanyu184212B compared to DMI-AdLacZ group. Our findings reveal that Hduanyu184212B overexpression interacts with AKAP12 and downregulate TXNIP in diabetic rats following acute MI.

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