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Title: Downregulation of miR-103a-3p Contributes to Endothelial Progenitor Cell Dysfunction in Deep Vein Thrombosis Through PTEN Targeting. Author: Zhang P, Zhao Q, Gong K, Long Y, Zhang J, Li Y, Guo X. Journal: Ann Vasc Surg; 2020 Apr; 64():339-346. PubMed ID: 31639479. Abstract: OBJECTIVE: Bone-marrow-derived endothelial progenitor cells (EPCs) can accelerate the dissolution of thrombi. However, EPC functions are weakened in deep vein thrombosis (DVT), and miR-130a-3p is downregulated in DVT. As little is known about the function of miR-130a-3p in EPCs, we aimed to explore the effects of miR-130a-3p on EPC functions and the mechanisms of miR-130a-3p regulation of EPCs in DVT. METHODS: The EPCs were transfected with miR-130a-3p mimics or miR-130a-3p inhibitor. Migration and angiogenesis of EPCs were detected by wound healing, Transwell, and tube formation assays. Dual luciferase assay was used to test the relation of miR-130a-3p and phosphatase and tensin homolog (PTEN). Protein and mRNA levels of associated genes were measured by western blotting (WB) and qRT-PCR. RESULTS: miR-103a-3p could promote EPC migration and angiogenesis, and it was also downregulated in EPCs isolated from DVT patients. Moreover, PTEN was a target of miR-130a-3p. Upregulation of PTEN rescued the auxoaction of miR-130a-3p in EPC function. CONCLUSIONS: Downregulation of miR-103a-3p contributes to EPC dysfunction in DVT via targeting PTEN. Thus, miR-130a-3p may be a potential target for DVT treatment.[Abstract] [Full Text] [Related] [New Search]