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Figure 1 | Fibrogenesis & Tissue Repair

Figure 1

From: Loss of PPARγ expression by fibroblasts enhances dermal wound closure

Figure 1

The deletion of PPARγ in skin fibroblasts. (A) Mice homozygous for loxP-PPARγ and hemizygous for an allele enabling a tamoxifen-dependent cre recombinase to be expressed under the control of a fibroblast-specific collagen type I promoter/enhancer were injected with tamoxifen or corn oil to generate mice deleted (K/K) or not (C/C) for PPARγ in fibroblasts. PCR genotyping of PPARγ WT (C/C) or PPARγ KO (K/K) mice. The upper panel shows the PCR result using primers detecting cre (approximately 650 bp band); the bottom panel shows the PCR result with specific primers which amplify Exon I and Exon II-deleted PPARγ after tamoxifen injection (approximately 350 bp band). (B) Western blot analysis of WT (C/C) and PPARγ KO (K/K) fibroblasts with an anti-PPARγ antibody. (C) Indirect immunofluorescence analysis of WT (C/C) and PPARγ KO (K/K) mice skin samples (original magnification × 40, bar = 25 μm) using an anti- PPARγ antibody. Red = PPAR gamma; Blue = DAPI. DAPI, 4',6-diamidino-2-phenylindole; PPARγ, peroxisome proliferator-activated receptor-γ.

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