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LncRNA TUG1 regulates FGF1 to enhance endothelial differentiation of adipose‐derived stem cells by sponging miR‐143
Author(s) -
Xue YaNan,
Yan Yu,
Chen ZiZi,
Chen Jia,
Tang FengJie,
Xie HuiQing,
Tang ShiJie,
Cao Ke,
Zhou Xiao,
Wang AiJun,
Zhou JianDa
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.29232
Subject(s) - cd31 , angiogenesis , matrigel , stem cell , microbiology and biotechnology , downregulation and upregulation , fgf1 , chemistry , biology , fibroblast growth factor , cancer research , biochemistry , gene , receptor , fibroblast growth factor receptor
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.