LAUSR

In the pathological mechanism of pulmonary arterial hypertension, the role of apoptosis‐resistant pulmonary microvascular endothelial cells (PVECs/AR) has been emphasized on the pulmonary vascular remodeling. In the present study, we investigated whether PVECs/AR can promote the proliferation and migration of pulmonary arterial smooth muscle cells (PASMCs), and to study the role of miR‐195‐5p in the crosstalk between these two types of cells. We confirmed that PVECs/AR can promote the proliferation and migration of PASMCs in a co‐culture system of AR/PVECs and PASMCs. Additionally, after exposure to hypoxia for 12 or 24 h, AR/PVECs had a higher mature miR‐195‐5p level than PVECs (P < 0.05, 12 and 24 h). Luciferase reporter assays were used to validate indications of the existence of an HRE in the miR‐195‐5p promoter. Knocking down Smad7 can reverse the inhibition of Lv‐S195 on TGF‐β1‐induced PASMCs remodeling. TGF‐β1 promoted cell growth in PASMCs, and the supernatant of PVECs/AP infected with Lv‐S195 inhibited TGF‐β1 enhanced proliferation in PASMCs, which was also blocked by Lv‐shRNA‐Smad7. The result of this experiment confirmed the specificity of the HIF‐1a/miR‐195/Smad7 pathway. Our data indicate the possible function of PVECs/AR in the process of pulmonary vascular remodeling. MiRNA‐195‐5p played a role as an interacting paracrine factor between PVECs/AR and PASMC, which seemed to function through the HIF‐1a/miRNA‐195‐5p/Smad7 pathway.