4.5 Article

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

Journal

JOURNAL OF CARDIOVASCULAR TRANSLATIONAL RESEARCH
Volume 10, Issue 2, Pages 209-220

Publisher

SPRINGER
DOI: 10.1007/s12265-017-9734-4

Keywords

Gene therapy; Cardiovascular disease; Myocardial infarction; AKAP12; VEGF

Funding

  1. NIH [HL69910]

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We examined the effects of overexpressing HSPA12B on angiogenesis and myocardial function by intramyocardial administration of adenovirus encoding HSPA12B (Ad. HSPA12B) 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 MI + Ad. HSPA12B, diabetic sham (DS) + Ad. LacZ, diabetic MI + Ad. LacZ and diabetic MI + Ad. HSPA12B. Following MI or sham surgery, the respective groups received either Ad. LacZ or Ad. HSPA12B via intramyocardial injections. We observed increased capillary and arteriolar density along with reduced fibrosis and preserved heart functions in DMI-AdHSPA12B compared to DMI-AdLacZ group. Western blot analysis demonstrated enhanced HSPA12B, 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-AdHSPA12B compared to DMIAdLacZ group. Our findings reveal that HSPA12B overexpression interacts with AKAP12 and downregulate TXNIP in diabetic rats following acute MI.

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