Anti-PIK3R2 monoclonal antibody, clone U26

Deep vein thrombosis (DVT) is a common complication of surgery. Endothelial progenitor cells (EPCs) are recruited into resolving venous thrombi. In this report, we investigated the effects of miR-126 on EPCs function and venous thrombus resolution. We demonstrated that overexpression of miR-126 enhanced EPCs' migration and tubulogenic activity in vitro, and promoted EPCs' homing and thrombus resolving in vivo. Moreover, we identified that miR-126 directly targeted PIK3R2 and affected PI3K/Akt signaling axis. Overall, our findings demonstrated that miR-126 promoted EPCs function through suppressing PIK3R2 expression and modulation of miR-126 may represent a potential therapeutic intervention for treating DVT. J. Cell. Biochem. 116: 1613-1623, 2015. (c) 2015 Wiley Periodicals, Inc.

OBJECTIVE: In the clinic, therapeutic options for pulmonary arterial hypertension are limited; therefore, investigating the therapeutic strategies and novel therapies is critical for pulmonary arterial hypertension (PAH) treatment. This study aimed to evaluate the role of miRNA-126 (miR-126) and its associated signaling pathways and specific mechanisms for the pathogenesis of PAH. MATERIALS AND METHODS: The pulmonary artery endothelial cells (PAECs) were isolated and identified. The miR-126 mimic and miR-126 inhibitor were synthesized. LV-3-miR-126 mimic viral vector and LV-3-miR-126 inhibitor vector were established and infected into pulmonary artery endothelial cells. Expression of sprouty-related EVH1 domain-containing protein 1 (SPRED1), phosphoinositide-3-kinase regulatory subunit 2 (PIK3R2) and miR-126 were detected using Real- time PCR (RT-PCR). Cell apoptosis (Annexin V-PE/7-AAD) and proliferation (PKH26) were examined by using FACScan flow cytometry. Vascular endothelial growth factor (VEGF), transforming growth factor beta 1 (TGF-beta 1) and TGF-beta 3 levels were evaluated using enzyme-linked immunosorbent assay (ELISA) kits. RESULTS: miR-126 inhibited the endothelial cells related to SPRED1 and PIK3R2 expression. Over-expression of miR-126 significantly inhibited the PAECs apoptosis compared to PAECs and blank LV-3 vector group (p<0.05). miR-126 significantly triggered the PAECs proliferation compared to PAECs and blank LV-3 vector group (p<0.05). In functional analysis, miR-126 mimic significantly increased the cells amounts of S phases compared to PAECs and blank LV-3 vector group (p<0.05). Pre-infection with miR-126 mimic significantly enhanced the levels of VEGF, TGF-beta 1, and TGF-beta 3 compared to PAECs and blank LV-3 vector group (p<0.05). CONCLUSIONS: miR-126 could affect cell apoptosis, proliferation, cell cycle, and modulate VEGF/TGF-beta levels.