皮肤瘢痕是皮肤创伤后纤维性修复的产物，如何预防瘢痕形成一直是困扰外科学界的难题。诸多研究集中于生长因子与瘢痕形成的关系，但终未能解决问题。该研究从再生医学的角度提出通过模拟胚胎皮肤无瘢痕愈合的相关因素将纤维性修复转化为再生修复的观点。即采用Smad3基因敲除小鼠（不能传导TGF-β信号）为动物模型来模拟胚胎皮肤的低TGF-β环境，在其皮肤创伤后将GFP转基因小鼠的毛囊干细胞移植于其伤口，为伤口提供可以分化为表皮及皮肤附属结构的干细胞，以此来模拟胚胎皮肤的再生。通过该模型研究抑制TGF-β作用效应联合毛囊干细胞移植是否能促进皮肤再生，从而减少瘢痕形成，这一问题的解答将为发展出新的抗瘢痕策略提供理论基础。在此基础上，我们将进一步在能够转导TGF-β信号的正常小鼠伤口中，局部应用TGF-β拮抗剂并联合毛囊干细胞移植，观察其能否促进皮肤再生、减少伤口瘢痕，为临床应用奠定基础。

Scar forms after skin wound healing which is can not be prevented. Previsously, many researchers focusing on the relative cytokines to get rid of scars proved little use.The phenomenon that an embryo skin which has low concentration of TGF-β repairs its wounds without scar illuminates our research to imitate this phenomenon to change scaring process to skin regeneration process. We transplant GFP Transgenic mouse hair follicle stem cells which can develop into epidermis and skin appendages into the wound of a Smad3-knockout mouse (TGF-β signaling is blocked) in order to imitate embryo skin regeneration microenvironment.This model which combines low TGF-β effect with stem cell transplantion to reduce scar formation maybe will provide a theory support for anti-scaring wound healing.As a result, we can furtherly use TGF-antagonists to block the TGF-β signling of a wild type mouse in its wound locally and transplant stem cells into its wound to observe the wound healing and scar formation,this part of the study will be helpful for clinical use in the future.