Airway smooth muscle—its relationship to the extracellular matrix

• Published in: Respiratory physiology & neurobiology Vol. 137; no. 2; pp. 339 - 346
• Main Authors: Black, Judith L., Burgess, Janette K., Johnson, Peter R.A.
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 16.09.2003
• Subjects: Adaptation, Physiological; Airways, smooth muscle; Animals; Asthma - physiopathology; Bronchi - cytology; Bronchi - metabolism; Disease, asthma, airway smooth muscle remodeling; Enzymes, metalloproteases; Extracellular Matrix - metabolism; Extracellular Matrix Proteins - metabolism; Humans; Mammals, humans; Matrix Metalloproteinases - metabolism; Mediators, connective tissue growth factor, CTGF; Mediators, TGFβ; Muscle, smooth, airway; Myocytes, Smooth Muscle - metabolism; Proteins, extracellular matrix; Trachea - cytology; Trachea - metabolism; Proteins, extracellular matrix; Enzymes, metalloproteases; Mammals, humans; Airways, smooth muscle; Muscle, smooth, airway; Mediators, TGFβ; Disease, asthma, airway smooth muscle remodeling; Mediators, connective tissue growth factor, CTGF
• ISSN: 1569-9048; 1878-1519
• DOI: 10.1016/S1569-9048(03)00157-5

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 TGFβ 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.