Wnt signalling inhibits adipogenesis in orbital fibroblasts from patients with Graves' orbitopathy

Br J Ophthalmol. 2022 Jul;106(7):1019-1027. doi: 10.1136/bjophthalmol-2020-316898. Epub 2021 Jun 30.

Abstract

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.

Keywords: experimental and laboratory; orbit.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipogenesis
  • Cell Differentiation
  • Cells, Cultured
  • Cyclin D1 / metabolism
  • Fibroblasts / metabolism
  • Graves Ophthalmopathy* / metabolism
  • Humans
  • Orbit / metabolism
  • Wnt Proteins
  • beta Catenin / metabolism

Substances

  • Wnt Proteins
  • beta Catenin
  • Cyclin D1