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

METHODSFibroblasts 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).

RESULTSIn 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).

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