LncRNA TUG1 regulates FGF1 to enhance endothelial differentiation of adipose‐derived stem cells by sponging miR‐143

Adipose‐derived stem cells (ADSCs) have emerged as a cell source for regeneration medicine. ADSCs possess the capacity to differentiate into endothelial cells and serve an essential role in vascular development and function. LncRNA taurine upregulated gene 1 (TUG1) has recently been linked with angiogenesis in hepatoblastoma. However, the roles of TUG1 in endothelial differentiation of ADSCs remain unidentified. Human adipose‐derived stem cells (hADSCs) were obtained and characterized by flow cytometry, Oil red O and Alizarin Red staining. HADSCs were maintained in the endothelial differentiation medium and the expressions of TUG1, miR‐143, and FGF1 were examined by qRT‐PCR. To assess endothelial differentiation, the expressions of CD31, von Willebrand factor (vWF), VE‐cadherin were examined by Western blot analysis, qRT‐PCR, and immunofluorescence. Tube formation in Matrigel was examined. The interactions between TUG1 and miR‐143, miR‐143 and FGF1 were validated by luciferase assays. During the endothelial differentiation process, TUG1 and FGF1 were upregulated, whereas miR‐143 was downregulated. TUG1 overexpression downregulated miR‐143, upregulated FGF1, CD31, vWF, and VE‐cadherin, and enhanced capillary tube formation. Luciferase assays showed that TUG1 interacted with miR‐143, and FGF1 was a direct target of miR‐143. Furthermore, the enhancement of endothelial differentiation induced by TUG1 overexpression was abolished by miR‐143 overexpression. Our findings implicated that lncRNA TUG1 promoted endothelial differentiation of ADSCs by regulating the miR‐143/FGF1 axis. 1) LncRNA taurine upregulated gene 1 (TUG1) and FGF1 were upregulated whereas miR‐143 was downregulated during the endothelial differentiation process of adipose‐deprived stem cells (ADSCs). 2) LncRNA TUG1 overexpression promoted endothelial differentiation of ADSCs. 3) LncRNA TUG1 acted as a sponge of miR‐143 and FGF1 was a direct target of miR‐143. 4) miR‐143 overexpression abolished the enhancement of endothelial differentiation induced by TUG1 overexpression.