上海交通大学学报（医学版）

上海交通大学学报（医学版）

• 论著（基础研究） • 上一篇    下一篇

脂肪干细胞来源的条件培养基对TGF-β1共同干预下的真皮成纤维细胞致纤维化能力的影响

宋菲1，原博2   

  1. 上海交通大学 医学院附属瑞金医院 1.上海市烧伤研究所，2.烧伤整形科，上海 200025
  • 出版日期:2017-05-28 发布日期:2017-05-31
  • 作者简介:宋菲（1982—），女，主管技师；电子信箱：mryuki@tom.com。
  • 基金资助:

    国家自然科学基金（81101433）

Effect of adipose stem cells derived conditioned medium on fibrogenesis of dermal fibroblasts co-stimulated by transforming growth factor-β1

SONG Fei1, YUAN Bo2   

  1. 1.Shanghai Burns Institute, 2.Department of Burns and Plastic Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China
  • Online:2017-05-28 Published:2017-05-31
  • Supported by:

    National Natural Science Foundation of China, 81101433

PDF (PC)

1471

摘要：

目的 ·探求脂肪干细胞来源的条件培养基（ASCs-CM）对转化生长因子β1（TGF-β1）共同干预作用下真皮成纤维细胞致纤维化能力的影响，初步明确脂肪干细胞参与调控真皮组织修复的旁分泌途径及内在机制。方法 ·在TGF-β1共同刺激下，用不同浓度的ASCs-CM干预真皮成纤维细胞，观察成纤维细胞增殖和凋亡，检测平滑肌肌动蛋白α（α-SMA）、Ⅰ型胶原蛋白（COL-1）、Ⅲ型胶原蛋白（COL-3）、肝细胞生长因子（HGF）及碱性成纤维细胞生长因子（FGF-2）mRNA水平和蛋白表达。观察HGF抗体对ASCs-CM+ TGF-β1促成纤维细胞凋亡的影响。结果 · ASCs-CM可抑制TGF-β1刺激下的成纤维细胞增殖，促进其凋亡；10% ASCs-CM+TGF-β1可抑制成纤维细胞α-SMA的表达；100% ASCs-CM+ TGF-β1可促进成纤维细胞胶原尤其是COL-3的表达，亦可提高HGFmRNA水平。HGF抗体可抑制100% ASCs-CM+ TGF-β1促成纤维细胞凋亡的作用。结论 ·脂肪干细胞或可通过旁分泌途径对TGF-β1干预作用下真皮成纤维细胞致纤维化能力产生影响，高浓度的ASCs-CM能促进胶原合成和分泌，同时又能抑制细胞增殖，促进凋亡。

关键词: 脂肪干细胞；成纤维细胞；细胞凋亡；肝细胞生长因子；转化生长因子&beta, 1

Abstract:

 Objective · To clarify effect of adipose stem cells derived conditioned medium (ASCs-CM) on fibrogenesis of dermal fibroblasts co-stimulated by transforming growth factor-β1 (TGF-β1), and explore the possible paracrine pathway of ASCs in regulating the dermal tissue rehabilitation. Methods · Co-stimulated by TGF-β1, dermal fibroblasts were treated with different concentrations of ASCs-CM. Various cellular events including cell proliferation, apoptosis, and mRNA and (or) protein levels of α-smooth muscle actin (α-SMA), type Ⅰ collagen (COL-1) , type Ⅲ collagen (COL-3), hepatocyte growth factor (HGF), basic fibroblast growth factor (FGF-2) were explored. Furthermore, the effect of HGF antibody on apoptosis of fibroblasts caused by ASCs-CM and TGF-β1 were also observed. Results · ASCs-CM inhibited fibroblasts proliferation caused by TGF-β1 and lead to cell apoptosis. α-SMA expression in fibroblasts was attenuated by 10% ASCs-CM +TGF-β1. It was demonstrated that 100% ASCs-CM with TGF-β1 had promoted collagens (especially COL-3) expression in fibroblasts, and increased HGF mRNA level as well. HGF antibody inhibited fibroblasts apoptosis produced by 100% ASCs-CM and TGF-β1. Conclusion · ASCs may have an effect on fibrogenesis of dermal fibroblasts co-stimulated by TGF-β1 through a paracrine way. High concentration of ASCs-CM not only increases collagen production and secretion, but also inhibits fibroblasts proliferation and accelerates apoptosis.

Key words: adipose-derived stem cells, fibroblasts, apoptosis, hepatocyte growth factor, transforming growth factor-β1