RESUMO
Peroxisome proliferator-activated receptors (PPARs) belong to the nuclear hormone receptor family of ligand-inducible transcription factors. Our previous study has shown that in human umbilical vein endothelial cells PPARβ initiates a protective mechanism that limits the extent of damage due to H2O2-induced injury. Although fibroblasts are one of the main cell types involved in wound repair, the role of PPARβ in the fibroblast response to heat injury has not been investigated. Thus, in this study, we examined possible protective role of PPARβ in fibroblasts from heat injury. We developed a novel dermal fibroblast heat injury model to characterize the mechanisms of the heat injury healing response that involved PPARβ. The specific PPARβ ligand GW0742, a PPARβ activator and a short hairpin RNA (shRNA) plasmid against PPARβ were used to reveal the action mechanism of PPARβ in heat injury-induced fibroblast changes in morphology and increased proliferation. In response to heat injury (52˚C for 30 s), fibroblast activation of PPARß, increased 1.56-fold. Administration of GW0742 significantly induced a protective effect on heat injury-induced fibroblasts by minimizing the structural damage and increasing the cell proliferation response. Likewise, inhinition of PPARß, usingh shRNA exacerbated the damage by inhibiting the de novo synthesis of PPARß. These results indicated that heat injury enhanced PPARß expression and PPARß protected fibroblast structure and proliferation.