RT Journal Article
SR Electronic
T1 Wnt signalling inhibits adipogenesis in orbital fibroblasts from patients with Graves’ orbitopathy
JF British Journal of Ophthalmology
JO Br J Ophthalmol
FD BMJ Publishing Group Ltd.
SP 1019
OP 1027
DO 10.1136/bjophthalmol-2020-316898
VO 106
IS 7
A1 Sang Joon Jung
A1 Yeon Jeong Choi
A1 Tae Kwann Park
A1 Sang Earn Woo
A1 Bo-Yeon Kim
A1 Jin Sook Yoon
A1 Sun Young Jang
YR 2022
UL http://bjo.bmj.com/content/106/7/1019.abstract
AB 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.Data are available upon reasonable request.