中文摘要：

目的探讨β1转化生长因子（transforming growth factorp1，TGF-β1）诱导入表皮干细胞（human epidermal stemcells，hESCs）分化与瘢痕形成之间存在的关联。方法将包皮环切术后的包皮用中性蛋白水解酶消化，采用改良的Ⅳ型胶原选择黏附法分离、培养，传代至第3代时经过hESCs表面标志物β1整合素和CK19检测，证实为hESCs后接种于24孔板，随机分为3组：3d组、7d组、空白对照组，前两组分别加入梯度浓度的TGF-β1（0．1、5．0、10．0ng／m1）诱导，采用HE常规染色及Masson胶原特殊染色、免疫组织化学染色等手段检测量波形蛋白表达和羟脯氨酸试剂盒法测量各组上清液中胶原含量。结果hESCs在TGF-β1诱导下，形态由圆形转变为梭形类成纤维细胞样，Masson胶原染色阳性，释放到细胞上清液中的胶原浓度，均显著高于对照组，抗-波形蛋白染色阳性率各组都至少在（95．00±1．20）％以上，大于对照组的（5．70±0．20）％（P〈0．05）。结论结果表明，hESCs与病理性瘢痕发生关系极其密切，在TGF-β1体外诱导下向成纤维细胞分化，分泌胶原，提示在病理性瘢痕的发生中，hESCs可能是活化的成纤维细胞的另一个来源，hESCs可能参与瘢痕增生发生过程。

英文摘要：

Objective To investigate the correlation between human epidermal stem cell （hESCs） and hypertrophic scar or keloid. Methods Improved collagen Ⅳ-coated adhesion methods was used to isolate and culture the epidermal stem cells after neutral protease selectively digested the dermo-epidermal junctions. After the cells were cultured and expanded in vitro, and passage 3 hESCs were induced by different concentrations of TGF 131 （0.1, 5.0, and 10.0 ng/ml）. Morphological features and identification of these cells were meseasured by HE, Masson, immunohistochemical staining on the days 3 and 7, respectively. Results After induced by TGF-β1 for 3 and 7 days, the morphology of the epidermal stem cell （hESCs） was changed into fusiform shape, similar to fibroblasts. 70 % of the cell which was induced by TGF-β1 were blue stained in the cytoplasm by Masson stain, which is the distinctive method for collagen, suggesting collagen appeared or increased in the cells. The collagen concentrations in supernatants of hESCs were 0. 4150 ± 0. 0014, 0. 3380 ± 0. 0020, and 0. 3870± 0. 0020, much higher than that in control group （0. 0780 ± 0. 0025） and normal skin fibroblast group （0. 1500± 0. 0051）（P〈0. 05）. Immunohistochemical staining revealed that positive rates of these cells for anti-vimentin staining were more than （95.00± 1.20）% in experiments and （5. 70±0.20） % in control group. Conclusion The differentiantion of hESCs induced by TGF-β1 into fibroblasts indicates that hESCs may play a role in the pathogenesis of hypetrophic scar and keloid.