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Objective:Previously researches showed that, the formation of the pathologic scar might be the transdifferentiation of HSF into MyoF, and the persistent existance of myofibroblast. TGF-β1 was recognized as the most important growth factor in the development of fibrosis, can promote the transdifferentiation of human hypertrophic scar fibroblast in vitro. Connective tissue growth factor(CTGF), the down regulator of TGF-β1, was first found in 1991, our study aims to investigate the role of connective tissue growth factor(CTGF) in the transdifferentiation of human hypertrophic scar fibroblast(HSF)-myofibroblast(MyoF), and the relationship with TGF-β1.Methods: The human HSF were cultured in the presence or absence of CTGF, TGF-β1 and CTGF ASODN, transdifferentiation of HSF into MyoF was assessed by microscopy, Immunocytochemical method, Western-blot and flow cytometry.Result: The morphology of HSF were all changed by the stimulation of CTGF or/and TGF-β1 for 48h, especially in the CTGF combined TGF-β1 group; For one thing, the sequence of the cells disordered; for another thing, unformed cells were increased; the third, a-SMA positive cells were increased.Western-blot showed that, there was a dose-dependent increase in the expression of a-SMA with increasing concentrations of CTGF and TGF-β1, while the CTGF’s concentration reached to 7.5ng/ml and TGF-β1’concentration reached to 10ng/ml, the expression of a-SMA no longer increase as the concentrations went up. Compared with CTGF group and TGF-β1 group, the expression of a-SMA in the CTGF combined TGF-β1 group showed a significant increase(P<0.05), and the transfection combined TGF-β1 group showed a significant decrease(P<0.05), compared with the TGF-β1 group.Flow cytometry showed that, the percentage of cells expressing a-SMA changed significantly, the percentage in control group was 10.76±2.81%, while in the CTGF group
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