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重组人 decorin 通过抑制 TGF-β1 诱导的增生性瘢痕成纤维细胞收缩胶原格子。

Recombinant human decorin inhibits TGF-beta1-induced contraction of collagen lattice by hypertrophic scar fibroblasts.

机构信息

Department of Burn and Plastic Surgery, Guangzhou Red Cross Hospital, Jinan University, Guangzhou, China.

出版信息

Burns. 2009 Jun;35(4):527-37. doi: 10.1016/j.burns.2008.08.021. Epub 2009 Jan 23.

Abstract

Decorin was reported to bind transforming growth factor-beta (TGF-beta(1)) and neutralise some of its activity as a key regulator of wound contraction and hypertrophic scar formation. In this study, we investigated whether recombinant human decorin affected TGF-beta(1)-induced fibroblast contractile activity, by using fibroblast-populated collagen lattice with decorin added to the collagen gel. Hypertrophic scar fibroblasts showed greater basal contraction of collagen gels than normal fibroblasts, and the addition of TGF-beta(1) significantly enhanced this. Decorin inhibited both the basal and TGF-beta(1)-enhanced contraction of collagen gel by both normal and hypertrophic scar fibroblasts. Decorin also inhibited TGF-beta(1)-induced alpha-smooth muscle actin (alpha-SMA), plasminogen activator inhibitor-1 (PAI-1) protein and mRNA expressions in normal and hypertrophic scar fibroblasts. These results suggest that decorin may have therapeutic potential for excessive skin contraction as observed in hypertrophic scarring.

摘要

已有报道称,核心蛋白聚糖(decorin)可与转化生长因子-β(TGF-β(1))结合,并中和其部分活性,而 TGF-β(1)作为调控创伤收缩和增生性瘢痕形成的关键因子之一。在本研究中,我们通过向胶原凝胶中添加富含纤维母细胞的胶原晶格,探究了重组人核心蛋白聚糖对 TGF-β(1)诱导的纤维母细胞收缩活性的影响。增生性瘢痕纤维母细胞对胶原凝胶的基础收缩能力强于正常纤维母细胞,且 TGF-β(1)的添加显著增强了这一作用。核心蛋白聚糖可抑制正常和增生性瘢痕纤维母细胞的基础收缩和 TGF-β(1)增强的胶原凝胶收缩。核心蛋白聚糖还可抑制 TGF-β(1)诱导的正常和增生性瘢痕纤维母细胞中α-平滑肌肌动蛋白(α-SMA)、纤溶酶原激活物抑制剂-1(PAI-1)蛋白和 mRNA 的表达。这些结果表明,核心蛋白聚糖可能具有治疗过度皮肤收缩的潜力,而过度皮肤收缩是增生性瘢痕形成的主要特征。

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