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瘢痕疙瘩中Smads表达的研究 被引量:7

Expression of Smads in keloid scarrin
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摘要 目的探讨不同类型Smads在瘢痕疙瘩、正常瘢痕和正常皮肤中的差异表达及其意义。方法采用RT-PCR和Western Blot法分别对10例瘢痕疙瘩、10例正常瘢痕及10例正常皮肤组织,以及体外培养瘢痕疙瘩、正常瘢痕及正常皮肤成纤维细胞中的Smads mRNA及蛋白的表达水平进行检测。用t检验比较其表达差异,P〈0.05为差异具有统计学意义。结果在瘢痕疙瘩组织及瘢痕疙瘩成纤维细胞中,Smad7的mRNA及蛋白水平表达明显低于正常瘢痕(P〈0.05)和正常皮肤(P〈0.05),而Smad2、3的mRNA及蛋白水平表达以及磷酸化的Smad2、3的蛋白水平表达并无明显改变(P〉0.05)。结论在瘢痕疙瘩中,存在有Smad7的表达缺陷,这可能是增高的转化生长因子-β1(TGF-β1)/Smads信号传导不能被自身负反馈循环终止的重要原因。 Objective To investigate the differential expression of different types of Smads in keloids, normal scars and normal skins and its possible clinicopathological significance. Methods RT-PCR and Western blot methods were used to examine the expression of Smads mRNA and proteins level in 10 cases of keloid, in 10 cases of normal scar and in 10 cases of normal skin tissues and fibroblasts. Fibroblasts of keloid, normal scar and normal skin were cultured in vitro. The expression difference were compared and analyzed by t-test, there was statistical difference when P 〈 0. 05. Results The mRNA and protein expression of inhibitory Smad7 were significantly down regulated in keloid compared with normal scar ( P 〈 0. 05 ) and normal skin ( P 〈 0. 05 ). However, no significant difference of the mRNA and protein expression of Smad2, 3 and the protein expression of phosphorylation of Smad2, 3 in keloid, normal scar, normal skin tissues and fibroblasts. Conclusions The decreased expression of Smad7 in keloid might play a significant role in the increased TGF-β1/Smads signal transduction, which can not be terminated by autologous negative feedback cycle.
出处 《中华外科杂志》 CAS CSCD 北大核心 2009年第12期941-943,共3页 Chinese Journal of Surgery
基金 广东省自然科学基金资助项目(07001657) 广东省医学科研基金资助项目(A2007042)
关键词 瘢痕疙瘩 基因表达 信号传导 转化生长因子Β1 Smads基因 Keloid Gene expression Signaling transduction Transforming growth factor betal Smads gene
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参考文献6

  • 1Ogawa R. Keloids as a serious disease such as malignancy. Plast Recortstr Surg, 2008, 122:993-994.
  • 2Robles DT, Moore E, Draznin M, et al. Keloids: pathophysiology and management. Dermatol Online J, 2007, 13:9.
  • 3Jagadeesan J, Bayat A. Transforming growth factor beta (TGFbeta) and keloid disease. Int J Surg, 2007, 5:278-285.
  • 4Bock O, Yu H, Zitron S, et al. Studies of transforming growth factors beta 1-3 and their receptors Ⅰ and Ⅱ in fibroblast of keloids and hypertrophic scars. Acta Derm Venereol, 2005, 85: 216 -220.
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  • 6Kopp J, Preis E, Said H, et al. Abrogation of transforming growth factor-beta signaling by SMAD7 inhibits collagen gel contraction of human dermal fibroblasts. J Biol Chem, 2005, 280: 21570- 21576.

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