Figure 4.

PPARγ2 acetylation at K382 regulates lipid accumulation. (a) Effect of Sirt7 KD on Oil Red‐O staining in adipocytes. C3H10T1/2 cells were infected with control and Sirt7 short hairpin RNA retrovirus. After selection by puromycin, C3H10T1/2 cells were differentiated into adipocytes for 5 days. Representative images of 3 independent experiments are shown. (b) Gene expression of Sirt1, Sirt7, Pparg2, and target genes for PPARγ2 in differentiated C3H10T1/2 adipocytes (n = 3). (c, d) Effect of PPARγ2 WT, PPARγ2^K382R, and PPARγ2^K382Q overexpression on Oil Red‐O staining in adipocytes. C3H10T1/2 cells were infected with control retrovirus or retroviruses expressing PPARγ2, PPARγ2^K382R, and PPARγ2^K382Q. After puromycin selection, the cells were differentiated into adipocytes for 5 days. Representative images (c) and expression of Pparg2 mRNA (d) from 3 independent experiments are shown. (e) Effect of PPARγ2^K382R overexpression on Oil Red‐O staining in adipocytes. Control and Sirt7 KD‐C3H10T1/2 cells were infected with retroviruses expressing PPARγ2^K382R, and the cells were differentiated into adipocytes for 5 days. (f) Expression of PPARγ2 target genes in differentiated C3H10T1/2‐derived adipocytes expressing PPARγ2^K382R and PPARγ2^K382Q (n = 3). Data are shown as the mean ± the standard error of the mean. *P < 0.05