Background: Pulmonary arterial hypertension (PAH) is a devastating disease and long non-coding RNAs (lncRNAs) are essential for PAH progression. Also, lncRNA plasmacytoma variant translocation 1 (PVT1) plays important roles in cell proliferation and migration, however, the effect of PVT1 on pulmonary artery smooth muscle cells (HPASMCs) in PAH remains unknown. This study aimed to determine the role and underlying mechanisms of PVT1 in HPASMCs.Methods: The results demonstrated that the expression of PVT1 was upregulated in pulmonary arterial tissues and HPASMCs and was positively correlated with pulmonary arterial pressure.Results: Knockdown and overexpression of PVT1 suppressed and promoted HPASMCs proliferation and migration, respectively. Mechanical and functional studies revealed that PVT1 functioned as a competing endogenous RNA of miR-140-5p and their expressions were negatively correlated.Conclusions: Knockdown of PVT1 did not suppress proliferation and migration in HPASMCs transfected with the miR-140-5p inhibitor. Moreover, fragile X-related proteins 1 (Fxr1) was identified as the target gene of miR-140-5p. Downregulation of PVT1 decreased the level of Fxr1 while this inhibitory effect was reversed by the miR-140-5p inhibitor. In conclusion, the upregulation of PVT1 promoted proliferation and migration in HPASMCs though the miR-140-5p/Fxr1 signaling pathway, indicating PVT1 may serve as a promising diagnostic biomarker for PAH.
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