Dataset Information


MiR-26b-5p/TCF-4 Controls the Adipogenic Differentiation of Human Adipose-derived Mesenchymal Stem Cells.

ABSTRACT: In this study, we assessed the ability of miR-26b-5p to regulate T cell factor 4 (TCF-4) expression and thereby control human adipose-derived mesenchymal stem cell (hADMSC) adipogenic differentiation. Adipogenic medium was used to induce hADMSC differentiation over a 6-d period. The ability of miR-26b-5p to interact with the TCF-4 mRNA was confirmed through both predictive bioinformatics analyses and luciferase reporter assays. Immunofluorescent staining was used to visualize the impact of miR-26b-5p inhibition or overexpression on TCF-4 and ?-catenin levels in hADMSCs. Further functional analyses were conducted by transfecting these cells with siRNAs specific for TCF-4 and ?-catenin. Adipogenic marker and Wnt/?-catenin pathway gene expression levels were assessed via real-time polymerase chain reaction and western blotting. ?-catenin localization was assessed via immunofluorescent staining. As expected, our adipogenic media induced the adipocytic differentiation of hADMSCs. In addition, we confirmed that TCF-4 is an miR-26b-5p target gene in these cells, and that protein levels of both TCF-4 and ?-catenin were reduced when these cells were transfected with miR-26b-5p mimics. Overexpression of this microRNA also enhanced hADMSC adipogenesis, whereas TCF-4 and ?-catenin overexpression inhibited this process. The enhanced hADMSC adipogenic differentiation that was observed following TCF-4 or ?-catenin knockdown was partially reversed when miR-26b-5p expression was inhibited. We found that miR-26b-5p serves as a direct negative regulator of TCF-4 expression within hADMSCs, leading to inactivation of the Wnt/?-catenin pathway and thereby promoting the adipogenic differentiation of these cells in vitro.


PROVIDER: S-EPMC7563810 | BioStudies | 2020-01-01

REPOSITORIES: biostudies

Similar Datasets

2013-01-01 | S-EPMC3739795 | BioStudies
2020-01-01 | S-EPMC7188903 | BioStudies
2016-01-01 | S-EPMC5130048 | BioStudies
1000-01-01 | S-EPMC5386366 | BioStudies
2019-01-01 | S-EPMC6426711 | BioStudies
2017-01-01 | S-EPMC6529121 | BioStudies
2017-01-01 | S-EPMC5228128 | BioStudies
1000-01-01 | S-EPMC4943694 | BioStudies
2019-01-01 | S-EPMC6700432 | BioStudies
2016-01-01 | S-EPMC4973152 | BioStudies