[The role of cell pathway in apoptosis of fibroblasts from proliferative scar induced by steroid or IFN]

Zhonghua Zheng Xing Wai Ke Za Zhi. 2008 Jan;24(1):46-9.
[Article in Chinese]

Abstract

Objective: This paper is to investigate the effects of steroid or IFN alpha-2b on apoptosis and cell pathway of fibroblasts from keloids, hypertrophic scars and normal skins and different responses of different fibroblasts.

Methods: 6 samples from keloid, hypertrophic scar and normal skin were collected respectively and fibroblasts from different sources were cultured in vitro. After different fibroblasts were treated with dexamethasone (0.1 mg/ml) or IFN alpha-2b (1000 U/ml), Bax and Bcl-2 protein expressions were detected in situ by immunohistochemical staining; DNA ladders of different fibroblasts were observed by gel electrophoresis; and relative activated (phospho-) ERK1/2 and JNK pathways were detected by method of FACE ELISA.

Results: Dexamethasone could induce apoptosis of fibroblasts from keloids, hypertrophic scars and normal skins through activating (phospho-) ERK1/2 and JNK pathways; IFN alpha-2b could not induce apoptosis of fibroblasts from different sources. IFN alpha-2b could inhibit (phospho-) ERK1/2 pathway and could not affect (phospho-) JNK pathways of fibroblasts from keloid and hypertrophic scar. IFN alpha-2b could affect neither (phospho-) ERK1/2 pathway nor (phospho-) JNK pathways of fibroblasts from normal skin.

Conclusions: The responses of different fibroblasts to steroid or IFN alpha-2b were different.

MeSH terms

  • Adult
  • Apoptosis / drug effects*
  • Cells, Cultured
  • Cicatrix, Hypertrophic / chemically induced
  • Cicatrix, Hypertrophic / metabolism*
  • Cicatrix, Hypertrophic / pathology
  • Female
  • Fibroblasts / metabolism*
  • Fibroblasts / pathology
  • Hormones / pharmacology
  • Humans
  • Interferon alpha-2
  • Interferon-alpha / pharmacology
  • Keloid / chemically induced
  • Keloid / metabolism*
  • Keloid / pathology
  • Male
  • Middle Aged
  • Recombinant Proteins
  • Signal Transduction

Substances

  • Hormones
  • Interferon alpha-2
  • Interferon-alpha
  • Recombinant Proteins