Glucose impairs angiogenesis and promotes ventricular remodelling following myocardial infarction via upregulation of microRNA-17.

Glucose impairs angiogenesis and promotes ventricular remodelling following myocardial infarction via upregulation of microRNA-17. Exp Cell Res. 2019 May 07;: Authors: Yan M, Chen K, Sun R, Lin K, Qian X, Yuan M, Wang Y, Ma J, Qing Y, Xu J, Wei M, Huang D, Li J Abstract Hyperglycaemia is known to impair angiogenesis, which may contribute to the poor prognosis of diabetic patients following myocardial infarction (MI). miR-17 has been reported to be involved in the proliferation, migration, and angiogenesis of a variety of vascular endothelial cells. However, how miR-17 regulates angiogenesis under hyperglycaemic conditions has not been reported. Thus, the aim of this study was to investigate the role of miR-17 in the impairment of angiogenesis induced by high glucose. In vitro, human umbilical vein endothelial cells (HUVECs) transfected with miR-17 mimics or inhibitors were incubated with normal-glucose or high-glucose (HG) medium. In vivo, miR-17 or negative control antagomirs were administered by tail vein injection in an MI model of streptozotocin (STZ)-induced diabetic mice. MiR-17 was upregulated, while VEGFA was downregulated in MI mice with diabetes and in HUVECs exposed to HG. The luciferase reporter gene assay confirmed that VEGFA is a target gene of miR-17. Moreover, inhibition of miR-17 prevented HG-induced VEGFA downregulation and impaired the capacity for migration and tube formation in HUVECs. Administration of miR-17 an...
Source: Experimental Cell Research - Category: Cytology Authors: Tags: Exp Cell Res Source Type: research