The Effect of Tumor Necrosis Factor-alpa on Type I Procollagen and Collagenase Gene Expression in Hypertrophic Scar and Keloid Fibroblast.

Shin, Seung Yup; Chang, Do Myung; Kim, Young Jin; Lee, Baek Kwon; Wee, Sung Shin; Ahn, Sang Tae

Search: J Korean Soc Plast Reconstr Surg Search

CLOSE

Original Article

Journal of the Korean Society of Plastic and Reconstructive Surgeons 2001;28(2):145-151.
Published online March 1, 2001.

The Effect of Tumor Necrosis Factor-alpa on Type I Procollagen and Collagenase Gene Expression in Hypertrophic Scar and Keloid Fibroblast.

Seung Yup Shin, Do Myung Chang, Young Jin Kim, Baek Kwon Lee, Sung Shin Wee, Sang Tae Ahn

Department of Plastic and Reconstructive Surgery, The Catholic University of Korea, College of Medicine.

Abstract

Recent studies have demonstrated that tumor necrosis factor-alpa(TNF-alpa) decreased production of type I and III procollagens and increased production of collagenase in cultured human dermal fibroblasts. The purpose of this study was to examine the effect of TNF-alpa on the level of expression of type I procollagen, collagenase mRNA in hypertrophic scar and keloid fibroblasts in culture. The cultured fibroblasts from normal skin, hypertrophic scar and keloid were exposed to 0, 1, 10, and 100 ng/ml of TNF-alpa for 24 hours. Then, type I procollagen mRNA and collagenase mRNA were measured by quantitative RT-PCR and quantified by computerized densitometry(TINA). In normal skin fibroblasts, TNF-alpa significantly decreased the level of type I procollagen mRNA and increased collagenase mRNA. The maximal inhibition for type I procollagen mRNA was noted at 100 ng/ml of TNF-alpa and maximal enhancement for collagenase mRNA was noted at 100ng/ml of TNF-alpa. In hypertrophic scar fibroblasts, TNF-alpa significantly decreased the level of type I procollagen mRNA and increased collagenase mRNA. The maximal inhibition for type I procollagen mRNA was noted at 100 ng/ml of TNF-alpa which was the same as normal skin fibroblasts but there were no significant differences among TNF-alpa treated groups for collagenase mRNA. In keloid fibroblasts, TNF-alpa also significantly decreased the level of type I procollagen mRNA and increased collagenase mRNA. The maximal inhibition for type I procollagen mRNA was noted at 100 ng/ml of TNF-alpa which was the same as normal skin and hypertrophic scar fibroblasts but there were no significant differences among TNF-alpa treated groups for collagenase mRNA. These results strongly suggested that TNF-alpa might have a role in preventing progression of fibroproliferative disease, such as hypertrophic scar or keloid, and that the most effective concentration of TNF-alpa was found in 100 ng/ml.

Keywords: TNF-alpa; Hypertrophic scar; Keloid; Procollagen; Collagenase

TOOLS