Background/Aims To investigate the role of Wnt signalling in adipogenesis using an in vitro model of Graves’ orbitopathy (GO).
Methods Orbital fat was obtained from patients with GO and non-GO participants for primary orbital fibroblast (OF) culture. Expression levels of Wnt5a, Wnt10b, β-catenin, phospho-β-catenin and cyclin D1 were compared between GO and non-GO OFs. These expression levels were also determined during adipogenesis of GO and non-GO OFs. The effects of a stimulator and inhibitor of Wnt signalling on adipogenesis of GO and non-GO OFs were investigated.
Results Western blotting analysis showed significant reductions in β-catenin and cyclin D1 and significant enhancement of phospho-β-catenin in OFs from patients with GO, compared with OFs from non-GO participants (p<0.05). Expression of Wnt5a, Wnt10b, β-catenin and cyclin D1 in OFs was highest on day 0, and then gradually declined after induction of adipogenic differentiation. The expression levels of PPARγ, C/EBPα and C/EBPβ were reduced in Wnt stimulator-treated OFs in a dose-dependent manner. Oil red O staining confirmed that a stimulator of Wnt inhibited adipogenesis in GO OFs.
Conclusion These results indicate that Wnt signalling inhibits adipogenesis in OFs from patients with GO and non-GO participants. Further studies are required to examine the potential of Wnt signalling as a target for therapeutic strategies.
- experimental and laboratory
Data availability statement
Data are available upon reasonable request.
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Contributors SJJ, TKP and SYJ were responsible for the conception and design of the study, as well as the intellectual content. YJC performed experiments. SEW, BYK, J-SY and SYJ revised the article critically for intellectual content. All authors read and approved the final manuscript.
Funding This work was supported by a National Research Foundation of Korea (NRF) grant funded by the government of Korea (MSIT) (No. 2020R1A2C4002095), and was partially supported by the Soonchunhyang University Research Fund.
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed.