c-Jun is increased in hypertrophic scar and inhibits apoptosis in fibroblasts

To detect the expression pattern of c-Jun in human hypertrophic scars and investigate its role in regulation of cell proliferation and apoptosis in fibroblasts and its underlying action mechanism. In this study, we examined the expression of c-Jun in hypertrophic scars and fibroblasts using quantitative real-time polymerase chain reaction and western blot analysis and investigated the functional role of c-Jun in fibroblasts through detecting cell proliferation and apoptosis using cell viability assay and flow cytometry. The results showed that the c-Jun was increased in human hypertrophic scar tissues and fibroblasts compared with the respective matched human normal skin tissues or human keratinocyte HaCat cells. Overexpression of c-Jun enhanced proliferation and reduced apoptosis in fibroblasts, however, knockdown of c-Jun resulted in a converse tendency. The c-Jun upregulation could induce PPARβ, PDK, pAKT, collagen I production and repress cleaved-caspase 3, caspase 8 and caspase 9 expression in fibroblasts. It is demonstrated that c-Jun contribute to proliferation and repress apoptosis in fibroblasts and the action mechanism is involved in activation of PPARβ/pAkt. Our findings provide an insight into hypertrophic scarring and a potential novel target for management of human hypertrophic scar.