LncRNA PVT1 targets miR-143-3p to modulate endothelial cell function and thereby participate in deep vein thrombosis (DVT) of the lower limbs

The aim of this study is to investigate the diagnostic value of long non-coding RNA PVT1 (LncRNA PVT1) in deep vein thrombosis (DVT) of the lower limbs, as well as its regulatory role in damaged endothelial cells. A total of 384 participants were enrolled, including 208 patients with DVT. 3mL venous blood were collected from each participant. Thrombosis location and severity were assessed via Doppler ultrasound or venography. An endothelial cell injury model was induced using 250 µM cobalt chloride (CoCl₂). Gene expression was evaluated using RT-qPCR, while cell function was assessed via CCK-8 assays and flow cytometry. Angiogenesis and inflammatory factor expression was measured by ELISA. Dual luciferase reporter assays validated gene-target relationships. LncRNA PVT1 was significantly upregulated in DVT patients and injured endothelial cells. LncRNA PVT1 positively correlated with D-dimer and C-reactive protein (CRP) expression, indicating risk factors for DVT induction. Treatment with CoCl₂ increased LncRNA PVT1 expression in endothelial cells, while si-PVT1 enhanced viability and reduced apoptosis in damaged endothelial cells. It also suppressed expression of angiogenesis-related factors (VEGF, FGF-2) and inflammatory cytokines (TNF-α, IL-6). miR-143-3p, a downstream target gene of LncRNA PVT1, is downregulated in DVT patients. The miR inhibitor counteracts the effects of si-PVT1 on damaged endothelial cell function and inflammatory levels. LncRNA PVT1 negatively regulates miR-143-3p, thereby suppressing endothelial cell activity and promoting apoptosis. This increases levels of angiogenesis factors and inflammatory mediators, contributing to DVT pathogenesis.