中国组织工程研究

中国组织工程研究 ›› 2010, Vol. 14 ›› Issue (11): 1927-1930.doi: 10.3969/j.issn.1673-8225.2010.11.007

• 皮肤粘膜组织构建 skin and mucosal tissue construction • 上一篇    下一篇

Smad3和转化生长因子β1在瘢痕疙瘩、增生性瘢痕及正常皮肤中的表达：48∶40∶40例标本病理检测

庞久玲1，马 征2，刘 军1，刘爱东2   

  1. 1河北医科大学附属唐山工人医院烧伤整形科，河北省唐山市063000；
    2河北唐山职业技术学院医学校区，河北省唐山市  063000
  • 出版日期:2010-03-12 发布日期:2010-03-12
  • 作者简介:庞久玲，女，1977年生，河北省唐山市人，汉族， 2005年承德医学院毕业，主管护师，主要从事病理性瘢痕形成机制及其防治的研究。lad303@163.com

Expressions of Smad3 and transforming growth factor beta 1 in keloid, hypertrophic scars and normal skins: A 48: 40: 40 sample pathological detection

Pang Jiu-ling1, Ma Zheng2, Liu Jun1, Liu Ai-dong2   

  1. 1Department of Burn and Plastic Surgery, Workers’ Hospital of Tangshan, Hebei Medical University, Tangshan  063000, Hebei Province, China;
    2Medical Campus of Tangshan Vocational and Technical College, Tangshan  063000, Hebei Province, China
  • Online:2010-03-12 Published:2010-03-12
  • About author:Pang Jiu-ling, Chief nurse, Department of Burn and Plastic Surgery, Workers’ Hospital of Tangshan, Hebei Medical University, Tangshan 063000, Hebei Province, China lad303@163.com

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摘要：

目的：与病理性瘢痕发生机制相关的Smad3/转化生长因子β1信号传递通路研究多集中在体外成纤维细胞的培养上，在瘢痕疙瘩中的表达少见报道。检测病理性瘢痕中Smad3和转化生长因子β1蛋白的表达，探讨其在病理性瘢痕发生及发展中的作用。

方法：实验标本均来自2004-06/2008-06河北医科大学附属唐山工人医院烧伤整形科手术患者，瘢痕疙瘩48例，年龄16~52岁；增生性瘢痕40例，年龄18~56岁；选取同期因其他手术切除的正常皮肤组织40例作为对照组。应用流式细胞术检测48例瘢痕疙瘩、40例增生性瘢痕及40例正常皮肤组织Smad3和转化生长因子β1的表达。

结果：Smad3和转化生长因子β1在瘢痕疙瘩和增生性瘢痕中的表达明显高于正常皮肤组织中的表达(P < 0.05)，Smad3和转化生长因子β1在瘢痕疙瘩和增生瘢痕中的表达差异无显著性意义(P > 0.05)。瘢痕疙瘩和增生性瘢痕中Smad3和转化生长因子β1表达呈正相关(r=0.489 2， P；r=0.471 0，P=0.002 2)，Smad3和转化生长因子β1在正常皮肤组织中的表达未见明显相关性(P=0.471 4)。=0.000 4

结论：Smad3和转化生长因子β1在病理性瘢痕中高表达，Smad3和转化生长因子β1的协同作用可能参与病理性瘢痕的发生发展。

关键词: 病理性瘢痕, 瘢痕疙瘩, 增生性瘢痕, Smad3, 转化生长因子&beta, 1, 流式细胞术, 皮肤组织工程

Abstract:

OBJECTIVE: Study regarding Smad3/transforming growth factor-β1 (TGF-β1) signal transduction in pathological scars mainly focus on in vitro cultured fibroblasts, however, the correlation study was rare on keloid. The aim of this study is to detect the expressions of Smad3 and TGF-β1, and investigate their relationship in pathogenesis and development of pathological scars.

METHODS: Experimental samples were obtained from the patients, who underwent burn and plastic surgery at the Department of Burn and Plastic Surgery, Workers’ Hospital of Tangshan, Hebei Medical University, from June 2004 to June 2008, including 48 patients with Keloid, aged 16-52 years, and 40 patients with hypertrophic scars aged 18-56 years. Normal skins from additional 40 cases were served as controls. The expressions of Smad3 and TGF-β1 protein in keloid, hypertrophic scars and normal skin were examined by flow cytometry.

RESULTS: The expression of Smad3 and TGF-β1 were obviously greater in the experimental group than that of the control group (P < 0.05), but the difference between keloid and hypertrophic scars had no significance (P > 0.05). There was a positive correlation between Smad3 and TGF-β1 in keloid and hypertrophic scars (r=0.489 2, P=0.000 4; r=0.471 0, P=0.002 2). No notable correlation was found between Smad3 and TGF-β1 in normal skins (P=0.471 4).

CONCLUSION: The expressions of Smad3 and TGF-β1 are up-regulated, and the synergism of Smad3 and TGF-β1 may promote the development in pathological scars.

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