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Research Article

MiR-130a in the adipogenesis of human SGBS preadipocytes and its susceptibility to androgen regulation

ORCID Icon, , , , &
Pages 197-205 | Received 17 Jan 2020, Accepted 26 Mar 2020, Published online: 09 Apr 2020
 

ABSTRACT

Objectives: Adipogenesis is the differentiation process generating mature adipocytes from undifferentiated mesenchymal stem cells. The differentiation can be inhibited by androgens, although knowledge about intracellular effectors of this inhibition is scarce. Recently, androgen-regulated microRNAs were detected as interesting candidates in this context. In this study, we analyse the role of miR-130a and miR-301 in the adipogenesis of human SGBS preadipocytes and whether they are prone to androgen regulation. Materials and Methods: microRNA expression during adipogenic differentiation with or without androgen stimulation was measured by qPCR. Putative target genes of miR-130a and miR-301 were identified by target database search and validated in luciferase reporter assays. Results: miR-130a and miR-301 are both significantly downregulated on day 3 and day 5 of adipogenic differentiation in comparison to day 0. Under androgen stimulation, a significant upregulation of miR-130a was detected after 7 days of adipogenesis lasting to day 14, while miR-301 did not change significantly until day 14. Luciferase reporter assays revealed the androgen receptor (AR), adiponectin (ADIPOQ) and tumour necrosis factor alpha (TNFα) as miR-130a target genes. Conclusions: miR-130a is an androgen-regulated microRNA that is downregulated during the early phase of adipogenesis and exerts its functions by regulating AR and ADIPOQ translation. These data may help to identify new signalling pathways associated with the androgen-mediated inhibition of adipogenesis.

Acknowledgments

This work was in part funded by a DFG (German research foundation) grant (GR-4469/1) to TG and HMB. The funding source played no role in the interpretation of the data. We acknowledge the financial support within the funding programme Open Access Publishing by the German Research Foundation (DFG).

CW, JJ and MK performed the experiments, analyzed the data and reviewed the manuscript. TG and HMB designed the experiments, analyzed the data and drafted the manuscript. MW designed the experiments and reviewed the manuscript. All authors read and approved the final version of this manuscript.

Disclosure statement

The authors have no conflicts of interest to disclose.

Additional information

Funding

This work was supported by the Deutsche Forschungsgemeinschaft [GR-4469/1].