Fig. 3: PPARγ T166 dephosphorylation regulates lipid synthesis activity of skin wound macrophages.

a UMAP and violin plots showing the PPARγ activity in macrophages from skin wound healing phase I and phase II. b Correlations between FAS-related gene expression pattern and transcriptional activity of CEBPδ, PPARγ and SREBF2 in skin wound macrophages. c Schematic illustration indicating the reporter plasmid structure (left), representative flow cytometry histograms showing the reporter fluorescence levels (right) (n = 4 biological replicates). d Representative immunoblot of phospho-T166-PPARγ (pPPARγ^T166) and total PPARγ in BMDMs treated with IL-10. β-actin was used as a loading control (n = 3 biological replicates). Data were analyzed by a one-way ANOVA followed by a Dunnett’s multiple-comparisons test. e Heatmap showing expression patterns of FAS-associated signature genes between PPARγ^+/+ and PPARγ^A/A BMDMs or skin wound macrophages (6 dpi). f Protein expression of ACC1 and FASN in BMDMs from PPARγ^+/+ or PPARγ^A/A mice in response to IL-10. β-actin was used as loading control. n = 3 biological replicates. g Representative pictures of BODIPY staining in PPARγ^+/+ and PPARγ^A/A BMDMs in response to IL-10. The lipid droplets were quantified (n = 5 biological replicates). Scale bar, 10 μm. Data were analyzed by a one-way ANOVA followed by a Tukey’s multiple comparisons test. h Lipid droplets in PPARγ^+/+ and PPARγ^A/A BMDMs were quantified by flow cytometry. Dashed line indicates peak of the fluorescent signal. i Lipid synthesis rate in PPARγ^+/+ and PPARγ^A/A BMDMs. The data represent the incorporation of ¹⁴C-glucose in the lipid fraction of n = 4 biological replicates per group. Unless specified otherwise, the data are presented as means ± s.e.m. (error bar) and compared using the two-tailed Student’s t test. Source data are provided as a Source Data file.