中文摘要：

目的 平滑肌细胞表型具有可塑性，在哮喘气道重建中，平滑肌细胞表型由收缩型向合成型转化。本研究探讨气道平滑肌细胞在转化生长因子-β1（TGF-β1）刺激下细胞表型转换的特异性标志物基质Gla蛋白（MGP）mRNA和主要纤维化蛋白Ⅰ、Ⅲ、Ⅴ的表达。方法 人气道平滑肌细胞体外原代培养，传2～3代后重新接种，实验组10组，给予TGF-β1 100μg／ml刺激，每组均设未予TGF-β1复管作为对照，其余培养条件相同，7d后90％的细胞融合，收获。RT-PCR方法研究平滑肌细胞MPG mRNA的表达，Western blot法分析胶原蛋白Ⅰ、Ⅲ、Ⅴ的表达水平。结果 经TGF-β1刺激后，气道平滑肌细胞表达MGP mRNA为（62．3±13．1）％，对照组MGP mRNA为（27．4±11．4）％，两组差异有统计学意义（P〈0．01），TGF-β1。刺激后的平滑肌细胞表达胶原蛋白Ⅰ、Ⅲ、Ⅴ分别为（灰度值）67．6±10．0，94．5±9．8，83．8±16．2，高于对照组的平滑肌细胞，差异有统计学意义（P〈0．01）。结论 TGF-β1促进气道平滑肌细胞表达MGP mRNA和胶原蛋白Ⅰ、Ⅲ、Ⅴ，后两者作为气道平滑肌细胞表型转化的早期标志物，表明平滑肌细胞存在由收缩型向合成型转化的趋势。可以认为TGF-β1与平滑肌细胞的相互作用促进了气道重建过程。

英文摘要：

Objective Bronchial asthma is a chronic inflammatory disorder. Long-term inflammation leads to varying degrees of structural changes in the airway wall known as airway reconstruction or remodeling. These structural changes are found in the airways of most patients with prolonged disease. After remodeling, the airway walls show the submucous membrane becomes thick with collagen deposition, and the smooth muscle cells show hyperplasia and hypertrophy. Smooth muscle cells are a vital component of the airway wall, and a major effector cell involved in the course of bronchial contraction. Smooth muscle cell hyperplasia and hypertrophy are important pathological changes in airway remodeling. This study investigated the expression of markers of human airway smooth muscle cells （ASMCs） phenotypic change, which were matrix Gla protein （MGP） and major fibrosis proteins, after in vitro treatment with transforming growth factor-β1 （TGF-β1 ）. Methods Human ASMCs were subjected to primary culture in vitro. Ten groups of cells were treated with 100 μg/ml of TGF-β1, while the cells in the control groups were treated with 10% fetal bovine serum. After being cultured for 7 d, the cells of both groups were harvested. MGP mRNA expression was detected by RT-PCR. Protein levels of collagen I , m and V were determined by Western blot analysis. Results Treated with TGF-β1 , airway smooth muscle cells expressed MGP mRNA greater than controls [ （62. 3 ± 13. 1 ） % vs （ 27.4 ± 11.4 ） %, P 〈 0. 01 ]. Also, airway smooth muscle cells stimulated by TGF-β1 produced more collagen Ⅰ ,Ⅲ and Ⅴ than the control group （P 〈0. 01 ）. Conclusions TGF-β1 induced expression of collagen Ⅲ and Ⅴ, which are early markers of the switch from a contractile to a synthetic phenotype in ASMCs. This induction is an indication that ASMCs have the potential to make this switch and that TGF-β1 is involved in airway remodeling.