Vascular remodeling is a characteristic pathological feature of hypertension, it can cause of increasing vascular resistance and decrease of compliance. Vascular smooth muscle cell (VSMCs) dysfunction is the important foundation of vascular remodeling. Increasing evidences have revealed that IncRNA is an important regulatory factor of VSMC function. In this paper, we explored the function of IncRNA TUG1 in vascular remodeling of hypertension. Here, we found that IncRNA TUG1 was highly expressed in aorta of spontaneously hypertensive rats (SHR) rats and promoted the proliferation and migration of VSMCs (SHR-VSMCs). Bioinformatics analyze showed that IncRNA TUG1 sequence had miR-145-5p binding sites. Luciferase reporter test, RNA pulldown and qRT-PCR showed that IncRNA TUG1 could bind miR-145-5p. Similarly, bioinformatics analyze found that FGFIO 3 'UTR contained miR-145-5p binding sites. Luciferase reporter test, qRT-PCR and Western blot were shown that miR-145-5p inhibited FGFIO expression by binding to its 3 'UTR. MIT showed that miR-145-5p inhibited and FGF10 promoted SHR-VMSCs proliferation and migration. Overexpression of miR-145-5p or knocking down of FGFIO after overexpresion of IncRNA TUG1 could rescue the proliferation and migration promoted by IncRNA TUG1. LncRNA TUG1 and FGF10 promoted and miR-145-5p suppressed the expression of beta-catenin, TCF and LEF in SHR-VSMCs. Therefore, IncRNA TUG1/miR-145-5p/FGF10 promotes the proliferation and migration of VSMCs in hypertensive state by activating the Wnt/beta-catenin pathway. (C) 2018 Published by Elsevier Inc.