MiR-221-3p is upregulated in acute pulmonary embolism complicated with pulmonary hypertension and promotes pulmonary arterial smooth muscle cells proliferation and migration by inhibiting PTEN.

Abstract

Pulmonary arterial smooth muscle cells (PASMCs) functions are associated with the pathogenesis of pulmonary hypertension (PH) which is a life-threatening complication of acute pulmonary embolism (APE). This study sought to explore the expression pattern of microRNA (miR)-221-3p in APE-PH patients and its role in PASMCs proliferation and migration. The clinical data and venous blood of APE-PH patients were collected. The expression levels of miR-221-3p and phosphatase and tensin homolog (PTEN) in serum were determined, followed by receiver operator characteristic curve analysis of miR-221-3p diagnostic efficacy. PASMCs were transfected with miR-221-3p mimics and PTEN-overexpressed vector, followed by assessment of cell viability, proliferation, and migration through cell counting kit-8, 5-ethynyl-2'-deoxyuridine, Transwell, and wound healing assays. The binding between miR-221-3p and PTEN 3'UTR region was testified by the dual-luciferase assay. miR-221 was upregulated in the serum of APE-PH patients and presented with good diagnostic efficacy with 1.155 cutoff value, 66.25% sensitivity, and 67.50% specificity. miR-221 was negatively correlated with PTEN in APE-PH patients. miR-221 overexpression facilitated PASMCs proliferation and migration in vitro. miR-221-3p bound to PTEN 3'UTR region to decrease PTEN protein levels. PTEN overexpression abolished the promotive role of miR-221-3p in PASMCs. Overall, miR-221-3p targeted PTEN to facilitate PASMC proliferation and migration.