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. 2009 Mar 23;184(6):817–831. doi: 10.1083/jcb.200809028

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© 2009 Chong et al.

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Figure 7. — Regulation of IL-1β signaling via PPARβ/δ during wound repair in KO mice. (A and B) Expression level of sIL-1ra (A) and icIL-1ra (B) in WT and KO fibroblasts. WT and KO primary fibroblasts were treated with PPARβ/δ ligand (100 nM GW501516 [GW]) and/or 10 ng/ml IL-1β. The mRNA (left) and protein (right) expression levels were measured by qPCR and ELISA, respectively. (C) Expression level of sIL-1ra in early wound biopsies of KO mice. Wound fluids and biopsies were collected at the indicated day post-wounding (days 1–3, n = 7; day 7, n = 4). Unwounded skin was used as control (ctrl; n = 4). sIL-1ra mRNA and protein levels were determined by qPCR and ELISA, respectively. (D) Expression of sIL-1ra, icIL-1ra, KGF, IL-6, and GMCSF mRNAs from laser capture microdissected (LCM) dermis of WT (n = 3) and KO (n = 4) wound biopsies. Indicated mitogenic factor mRNA levels were analyzed by qPCR and normalized to control ribosomal protein P0. (E) Expression levels of indicated factor mRNAs in vehicle (veh; carboxymethylcellulose)- and IL-1ra–treated (3 × 2.5 µg) wounds of KO and WT mice as compared with corresponding unwounded (control) skin. *, P < 0.05; **, P < 0.01; ***, P < 0.001. Data are mean ± SEM, n = 4.