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  • Title: [Transdifferentiation of fibroblasts into myofibroblasts in the skin lesion of systemic sclerosis: role of transforming growth factor β1 and its signal transduction].
    Author: Liu T, Hu XD.
    Journal: Nan Fang Yi Ke Da Xue Xue Bao; 2011 Nov; 31(11):1840-5. PubMed ID: 22126761.
    Abstract:
    OBJECTIVE: To explore the role of the fibroblast transdifferentiation into myofibroblasts (MFBs) in the pathogenesis of systemic sclerosis (SSc) and investigate the influence of transforming growth factor β(1) (TGF-β(1)) and blocking of its signal transduction on fibroblast transdifferentiation. METHODS: Fibroblasts derived from the skin lesions of SSc patients and normal skin tissue were cultured in vitro. The proportion of MFBs in the fibroblast culture was analyzed qualitatively using immunocytochemistry and quantitatively with ELISA for α-smooth muscle actin (α-SMA). The changes in fibroblast transdifferentiation were observed after addition of TGF-β(1) in the cell culture and after blocking the signal transduction of TGF-β(1). RESULTS: The fibroblasts isolated from SSc patients and control subjects showed a similar morphology. The mean number of cells positive for α-SMA in SSc group was significantly higher than that in the control group (P<0.01). As culture time extended, α-SMA levels of the two groups both increased gradually (P<0.01), but the increments were significantly greater in SSc group than in the control group at 24, 48, and 72 h (P<0.05 all). Addition of TGF-β(1) resulted in significantly increased α-SMA levels in both groups (P<0.05), and SSc group showed significantly higher α-SMA levels than the control group at 24, 48, and 72 h (P<0.01). In the presence of TGF-β(1), blocking of Smads, ERK/MAPK, and p38MAPK pathways, but not JNK/MAPK pathway, caused an obvious decrease in α-SMA levels in the fibroblasts in both groups. CONCLUSION: The fibroblasts in the skin lesion of SSc patients have strong potential of transdifferentiation into MFBs, and TGF-β(1) can promote this transdifferentiation process possibly involving Smads, and ERK/MAPK, and p38MAPK signalling pathways.
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