Abstract
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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 19087-19097 |
| Number of pages | 11 |
| Journal | Journal of Cellular Biochemistry |
| Volume | 120 |
| Issue number | 11 |
| DOIs | |
| State | Published - Nov 1 2019 |
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Keywords
- adipose-deprived stem cells
- endothelial differentiation
- FGF1
- LncRNA TUG1
- miR-143
ASJC Scopus subject areas
- Biochemistry
- Molecular Biology
- Cell Biology
Cite this
LncRNA TUG1 regulates FGF1 to enhance endothelial differentiation of adipose-derived stem cells by sponging miR-143. / Xue, Ya Nan; Yan, Yu; Chen, Zi Zi; Chen, Jia; Tang, Feng Jie; Xie, Hui Qing; Tang, Shi Jie; Cao, Ke; Zhou, Xiao; Wang, Ai Jun; Zhou, Jian Da.
In: Journal of Cellular Biochemistry, Vol. 120, No. 11, 01.11.2019, p. 19087-19097.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - LncRNA TUG1 regulates FGF1 to enhance endothelial differentiation of adipose-derived stem cells by sponging miR-143
AU - Xue, Ya Nan
AU - Yan, Yu
AU - Chen, Zi Zi
AU - Chen, Jia
AU - Tang, Feng Jie
AU - Xie, Hui Qing
AU - Tang, Shi Jie
AU - Cao, Ke
AU - Zhou, Xiao
AU - Wang, Ai Jun
AU - Zhou, Jian Da
PY - 2019/11/1
Y1 - 2019/11/1
N2 - 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.
AB - 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.
KW - adipose-deprived stem cells
KW - endothelial differentiation
KW - FGF1
KW - LncRNA TUG1
KW - miR-143
UR - http://www.scopus.com/inward/record.url?scp=85068610896&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85068610896&partnerID=8YFLogxK
U2 - 10.1002/jcb.29232
DO - 10.1002/jcb.29232
M3 - Article
C2 - 31264280
AN - SCOPUS:85068610896
VL - 120
SP - 19087
EP - 19097
JO - Journal of Cellular Biochemistry
JF - Journal of Cellular Biochemistry
SN - 0730-2312
IS - 11
ER -