In vitro wounding of airway smooth muscle cell monolayers increases expression of TGF-β receptors
In vitro wounding of airway smooth muscle cell monolayers increases expression of TGF-β receptors
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DOI：
10.1016/s1569-9048(02)00111-8
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发表时间：
2002-09-04
影响因子：
2.3
通讯作者：
Khalil, N
中科院分区：
文献类型：
--
作者：
Chen, G;Khalil, N
在哮喘恶化期间，存在支气管上皮细胞损伤和炎症细胞涌入。在这些情况下，蛋白酶和各种细胞因子的释放可能导致气道平滑肌细胞（ASMC）损伤。气道重塑是哮喘的一个特征性表现，但 ASMC 损伤在重塑中的作用尚不清楚。此前，我们证明了牛 ASMC 汇合单层的机械损伤导致了具有生物活性的转化生长因子-β（TGF-β1）的释放。反过来，诱导胶原蛋白 I 的表达。在本研究中，我们通过流式细胞术和 Western 分析检测到，机械损伤后，ASMC 的信号转导 TGF-β 受体 TbetaR-I 和 TbetaR-II 的表达增加。皮质类固醇是哮喘的标准治疗方法，地塞米松的存在可减少伤口诱导的 TGF-β1 释放以及胶原蛋白 1、纤连蛋白和 TbetaR-II 的表达。这些结果表明，ASMC 损伤可能在 TGF-β1 介导的气道纤维化中发挥重要作用，可以通过使用皮质类固醇来预防。 (C) 2002 Elsevier Science B.V. 保留所有权利。
During an exacerbation of asthma, there is bronchial epithelial cell injury and influx of inflammatory cells. In these instances, the release of proteases and various cytokines could lead to injury of the airway smooth muscle cells (ASMCs). Airway remodeling is a characteristic finding in asthma but the role of ASMC injury in remodeling is unknown. Previously, we demonstrated that mechanical wounding of confluent monolayers of bovine ASMCs resulted in the release of biologically active transforming growth factor-betal (TGF-beta1). which in turn, induced collagen I expression, In the present study, we demonstrate that after mechanical wounding, ASMCs had an increased expression of the signal transducing TGF-beta receptors TbetaR-I and TbetaR-II as detected by flow cytometry and Western analysis. Corticosteroids are standard therapy in asthma and the presence of dexamethasone decreased wound-induced release of TGF-beta1 and the expression of collagen 1, fibronectin, and TbetaR-II. These results suggest that ASMC injury may play an important role in airway fibrosis mediated by TGF-beta1, which can be prevented by the use of corticosteroids. (C) 2002 Elsevier Science B.V. All rights reserved.