Purchase this article with an account.
L. Wang, C. Wang, Z. Wu, H. Yang; Peroxisome Proliferator-Activated Receptor- Antagonist Inhibits Adipocyte Differentiation in Thyroid-Associated Ophthalmopathy. Invest. Ophthalmol. Vis. Sci. 2008;49(13):2293. doi: https://doi.org/.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Adipogenesis contributes to the pathogenesis of Thyroid-associated ophthalmopathy (TAO). This study was conducted to evaluate the role of peroxisome proliferator-activated receptor-γ (PPARγ) in TAO adipose differentiation and to observe the function of PPARγ antagonist GW9662 on adipocyte differentiation.
Samples of fat were obtained from TAO-affected orbits and normal orbits. PPARγ transcript and expression levels were contrasted between TAO and normal. The preadipocytes isolated and cultured from the samples were subjected to the differentiation protocol supplemented with PPARγ antagonist GW9662 for different concentration (0.1µM, 1µM, 10µM, 50µM) or PPARγ agonist rosiglitazone (10µM). The percentage of differentiating cells was assessed by oil red O staining, morphological changes, flow cytometric analysis and PPARγ transcript and expression levels.
Adipose tissues in TAO-affected orbits showed stronger expression of PPARγ than the ones in normal orbits. The cell viability was decreased under 50µM GW9662 treatment. About 12.3% of preadipocyte differentiated supplemented with simply differentiation medium. When subjected to PPARγ antagonist GW9662, adipocyte differentiation decreased and were dose dependent, which was 11.9%, 10%, 6.7% and 4.1% respectively, and the levels of PPARγ expression were reduced obviously in the concentration of 10µM and 50µM. When subjected to PPARγ agonist rosiglitazone, adipocyte differentiation occurred in up to 61.3%, and the levels of PPARγ were enhanced obviously.
PPARγ plays an important role in the development of TAO. PPARγ antagonist can reduced adipogenesis severely and could provide a novel therapy for TAO patients.
This PDF is available to Subscribers Only