Xiao Zhibo1, Zhang Miaobo. 1. Department of Plastic and Cosmetic Surgery, the Second Affiliated Hospital, Harbin Medical University, Harbin, Heilongjiang Province, China.
Abstract
OBJECTIVE: Clinical observations indicate that the irradiation of pulsed-dye laser (PDL) can inhibit keloid growth; however, the mechanism of this process is unknown. The aim of this study was to explore the molecular mechanism of the action of PDL on keloid fibroblasts. METHODS: Twenty patients with keloids were selected for this study. Fibroblasts were harvested from keloid tissue. Cell cycle distribution and apoptosis induction were analyzed by flow cytometry and with an antibody to Fas. The expression of apoptosis-related proteins (Fas, BCL-2, and p53) was measured by flow cytometry. RESULTS: Fibroblasts with laser irradiation and control fibroblasts displayed significant resistance to Fas-mediated apoptosis. Analysis of cell cycle distribution indicated that approximately 64% of control fibroblasts were in the proliferative periods of the cell cycle (G2 to M and S phases). However, most fibroblasts with laser irradiation were in the G0 to G1 phase. Fas and BCL-2 expression did not differ significantly between the 2 groups, but p53 expression was much higher in fibroblasts with laser irradiation than in control fibroblasts. CONCLUSION: It is suggested that differences in cell cycle distribution and p53 protein expression may partly account for the biologic mechanism of 595-nm PDL in treating keloid disease.
OBJECTIVE: Clinical observations indicate that the irradiation of pulsed-dye laser (PDL) can inhibit keloid growth; however, the mechanism of this process is unknown. The aim of this study was to explore the molecular mechanism of the action of PDL on keloid fibroblasts. METHODS: Twenty patients with keloids were selected for this study. Fibroblasts were harvested from keloid tissue. Cell cycle distribution and apoptosis induction were analyzed by flow cytometry and with an antibody to Fas. The expression of apoptosis-related proteins (Fas, BCL-2, and p53) was measured by flow cytometry. RESULTS: Fibroblasts with laser irradiation and control fibroblasts displayed significant resistance to Fas-mediated apoptosis. Analysis of cell cycle distribution indicated that approximately 64% of control fibroblasts were in the proliferative periods of the cell cycle (G2 to M and S phases). However, most fibroblasts with laser irradiation were in the G0 to G1 phase. Fas and BCL-2 expression did not differ significantly between the 2 groups, but p53 expression was much higher in fibroblasts with laser irradiation than in control fibroblasts. CONCLUSION: It is suggested that differences in cell cycle distribution and p53 protein expression may partly account for the biologic mechanism of 595-nm PDL in treating keloid disease.