Fig. 4: Blockage of PPARγ T166 phosphorylation improves skin wound healing.

a Schematic illustration indicating the phases of skin inflammation, tissue repair after injury. b Representative time-lapse photographs of skin wounds in PPARγ^+/+ and PPARγ^A/A mice over 12 dpi. c Wound area and closure rate in PPARγ^+/+ and PPARγ^A/A mice over 12 dpi (n = 5 per genotype). d Protein levels of p-PPARγ^T166 and PPARγ were determined by western blots using the wounds from 1, 6 and 12 dpi mice. Control, 1 dpi and 12 dpi, n = 3 biologically independent mice per condition. 6 dpi, n = 4 biologically independent mice. Data were analyzed by a one-way ANOVA followed by a Dunnett’s multiple-comparisons test. e Percentage of CD80⁺ and CD206⁺ macrophages in wound tissue of 1-, 6- and 12-dpi in PPARγ^+/+ and PPARγ^A/A mice within the CD45⁺ immune cell population. n = 3 biological replicates. f The quantification of wound area in PPARγ^+/+ and PPARγ^A/A mice after treatment with CL-lipo and Lipo control. n = 4 (PPARγ^+/+ and PPARγ^+/+ + CL), n = 7 (PPARγ^A/A and PPARγ^A/A + CL) biologically independent samples. Data were analyzed by a one-way ANOVA followed by a Tukey’s multiple comparisons test. g The scratch wound closure rate of DFs co-cultured with PPARγ^+/+ or PPARγ^A/A BMDMs for 24 h (n = 3 per group). Data were analyzed by a one-way ANOVA followed by a Dunnett’s multiple-comparisons test. h Representative flow cytometry histograms and quantifications of surface levels of CD163 and CD206 in PPARγ^+/+ and PPARγ^A/A BMDMs treated with IL-10 for 48 h. n = 3 biological replicates per group. Data were analyzed by a one-way ANOVA followed by a Tukey’s multiple comparisons test. 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.