雷帕霉素诱导成纤维细胞自噬在瘢痕疙瘩中的作用  

Effects of Rapamycin induced fibroblasts autophagy in keloid

作　　者：陈琳[1] 张曦[1] 苏映军[1] 余州[1] 雷蕾[1] 郭树忠[1] 马显杰[1] 

机构地区：[1]第四军医大学西京医院整形外科,陕西西安710032

出　　处：《中国美容整形外科杂志》2016年第2期114-117,共4页Chinese Journal of Aesthetic and Plastic Surgery

基　　金：国家自然科学基金

摘　　要：目的探讨瘢痕疙瘩与正常皮肤中，真皮成纤维细胞层自噬水平的差异，并研究自噬诱导剂雷帕霉素对瘢痕疙瘩成纤维细胞Collagen吸α-SMA表达的影响。方法收集瘢痕疙瘩和正常皮肤临床标本，免疫组化和WB检测自噬标志物LC3的表达；雷帕霉素处理成纤维细胞，检测细胞CollagenI及α-SMA表达。结果瘢痕疙瘩中，LC3表达高于正常皮肤；雷帕霉素可诱导成纤维细胞自噬，并降低细胞Collagen I及α-SMA的表达。结论自噬与瘢痕疙瘩发病相关，雷帕霉素诱导自噬可以显著影响成纤维细胞合成胶原及向肌成纤维细胞分化的特性，干预细胞自噬可能是一种有效的治疗瘢痕的途径。Objective To survey the differences of autophagy between keloid and normal skin （NS）, and to study the effects of autophagy inducer Rapamycin on the expression of Collagen I and α-SMA in keloid fibro- blasts. Methods The clinical specimens of keloid and NS were collected, the immunohistochemistry and Western blot were used to detect the expression of LC3 （the microtubule-associated protein 1 light chain 3 proteins）, an autophagy marker ; the expression of Collagen I and α-SMA in the fibroblasts treated by Rapamycin were detec- ted. Results The expression of LC3 in keloid was higher than that in NS. Rapamycin can induce fibroblast autophagy, furthermore decreases the expression of Collagen I and α-SMA. Conclusion Autophagy may associate with the pathogenesis of keloids. Rapamycin inhibits collagen I production and myofibroblasts differentiation from fibroblasts through the autophagy pathway, which suggests that autophagy may be a promising target for keloid therapy.

关 键 词：瘢痕疙瘩 自噬 雷帕霉素 成纤维细胞 COLLAGEN I Α-SMA 

分 类 号：R619.6[医药卫生—外科学]