Airway smooth muscle - its relationship to the extracellular matrix
Airway smooth muscle - its relationship to the extracellular matrix
复制标题
DOI：
10.1016/s1569-9048(03)00157-5
复制
发表时间：
2003-09-16
影响因子：
2.3
通讯作者：
Johnson, PRA
中科院分区：
文献类型：
--
作者：
Black, JL;Burgess, JK;Johnson, PRA
气道平滑肌细胞具有多种特性，这些特性赋予其积极参与炎症过程和重塑事件的能力，这伴随着严重的持续性哮喘。在这些特性中，其与细胞外基质（ECM）的关系是通过释放基质蛋白、基质金属蛋白酶（MMP）及其组织抑制剂（TIMP）与ECM相互作用。来自哮喘受试者的肌细胞增殖更快，释放不同的基质蛋白，响应于TGF β刺激产生更多的结缔组织生长因子（CTGF），这些变化可能影响气道平滑肌收缩和增殖。气道平滑肌表面上的整合素在肌细胞和ECM之间传递信号，但这些整合素的表达和/或功能在哮喘中是否改变尚不清楚。目前的治疗不太可能有效预防或逆转重塑，因此，了解其机制的病理生理学事件至关重要。(C)2003 Elsevier B. V.保留所有权利。
The airway smooth muscle cell has a variety of properties, which confer on it the ability to participate actively in the inflammatory process and the remodeling events, which accompany severe, persistent asthma. Among these properties is its relationship to the extracellular matrix (ECM) with which it interacts by releasing matrix proteins, matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs). Muscle cells derived from asthmatic subjects proliferate faster, release a different profile of matrix proteins, produce more connective tissue growth factor (CTGF) in response to TGFbeta stimulation and these changes may impact on airway smooth muscle contraction and proliferation. Integrins on the surface of the airway smooth muscle transduce signals between the muscle cell and the ECM, but whether the expression and/or function of these is altered in asthma is not known. It is unlikely that current therapy is effective in preventing or reversing remodeling, and therefore, understanding the pathophysiological events, which underlie its mechanism is critical. (C) 2003 Elsevier B.V. All rights reserved.