[Role of p38 mitogen activated protein kinase on cyclic stretch in human facial hypertrophic scar fibroblasts differentiation into myofibroblasts]

Zhonghua Kou Qiang Yi Xue Za Zhi. 2013 Oct;48(10):615-20.
[Article in Chinese]

Abstract

Objective: To explore the signal transduction mechanism of p38 mitogen activated protein kinase (p38MAPK) in human facial hypertrophic scar fibroblast (FB) differentiation into myofibroblasts (MFB).

Methods: Fibroblasts of primary culture were simple randomly assigned into two groups: cyclic stretch (control group) and cyclic stretch pre-treated with SB203580(experimental group). Expression of P-p38MAPK and α-smooth muscle actin (α-SMA) protein were examined using Western blotting and expression of transforming growth factor β1 (TGF-β1) mRNA and α-SMA mRNA were examined using reverse transcription PCR (RT-PCR).

Results: In control group, the expressions of α-SMA, p38MAPK, TGF-β1 mRNA and α-SMA mRNA (0 h: 0.134 ± 0.011, 0.239 ± 0.015, 0.214 ± 0.018, 0.252 ± 0.010; 6 h: 0.152 ± 0.014, 0.287 ± 0.016, 0.288 ± 0.011, 0.277 ± 0.013; 12 h: 0.172 ± 0.017, 0.320 ± 0.017, 0.335 ± 0.013, 0.297 ± 0.006) , were significantly increased with loading time (6 h>0 h; 12 h>0 and 6 h). In experimental group (pre-treated with SB203580), the expressions of α-SMA, p38MAPK, TGF-β1 mRNA,α-SMA mRNA (6 h: 0.116 ± 0.017,0.128 ± 0.016,0.134 ± 0.014,0.163 ± 0.009; 12 h: 0.149 ± 0.013,0.136 ± 0.018,0.144 ± 0.013,0.187 ± 0.010) on corresponding time decreased sharply compared with those in control groups (6, 12 h).

Conclusions: The human facial hypertrophic scar fibroblasts differentiation in response to cyclic stretch was mediated by p38MAPK phosporylation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / genetics
  • Actins / metabolism
  • Adolescent
  • Adult
  • Cell Transdifferentiation
  • Cells, Cultured
  • Child
  • Cicatrix, Hypertrophic / metabolism
  • Cicatrix, Hypertrophic / pathology*
  • Enzyme Inhibitors / pharmacology
  • Female
  • Fibroblasts / metabolism
  • Fibroblasts / pathology*
  • Humans
  • Imidazoles / pharmacology
  • Male
  • Myofibroblasts / pathology*
  • Phosphorylation
  • Pyridines / pharmacology
  • RNA, Messenger / metabolism
  • Random Allocation
  • Signal Transduction*
  • Stress, Mechanical
  • Transforming Growth Factor beta1 / genetics
  • Transforming Growth Factor beta1 / metabolism
  • Young Adult
  • p38 Mitogen-Activated Protein Kinases / metabolism*

Substances

  • ACTA2 protein, human
  • Actins
  • Enzyme Inhibitors
  • Imidazoles
  • Pyridines
  • RNA, Messenger
  • Transforming Growth Factor beta1
  • p38 Mitogen-Activated Protein Kinases
  • SB 203580