Abstract
Acute lung injury is characterized by a severe disruption of alveolo-capillary structures and includes a variety of changes in lung cell populations. Evidence suggests the occurrence of rupture of the basement membranes and interstitial matrix remodeling during acute lung injury. The dynamic equilibrium of the extracellular matrix (ECM) under physiological conditions is a consequence of the balance between the regulation of synthesis and degradation of ECM components. Matrix metalloproteinases (MMPs) represent a group of enzymes involved in the degradation of most of the components of the ECM and therefore participate in tissue remodeling associated with pathological situations such as acute lung injury. MMP activity is regulated by proteolytic activation of the latent secreted proenzyme and by interaction with specific tissue inhibitors of metalloproteinases. This review details our knowledge of the involvement of MMPs, namely MMP-2 and MMP-9, in acute lung injury and acute respiratory distress syndrome.
Highlights
Acute lung injury is characterized by lesions of both lung endothelial and alveolar epithelial cells leading in more severe cases to complete denudation of epithelial basement membranes
Re-epithelialization involves cellular proliferation and differentiation, but cellular locomotion as well. These processes are necessarily accompanied by digestion of the provisional matrix allowing its replacement by normal basement membranes, made of type IV collagen, laminin, and nidogen
Matrix metalloproteinases (MMPs) in vivo are a-2 macroglobulin, which is restricted in its sites of activity due to its large size, and the family of specific tissue inhibitor of MMPs (TIMPs), naturally occurring proteins inhibiting these proteases and produced by many cell types [6]
Summary
Acute lung injury is characterized by lesions of both lung endothelial and alveolar epithelial cells leading in more severe cases to complete denudation of epithelial basement membranes. During the acute inflammatory phase, basement membranes are damaged with deposition of a provisional extracellular matrix (ECM) made of fibrinogen, fibronectin, and fibrillar collagens. Re-epithelialization involves cellular proliferation and differentiation, but cellular locomotion as well These processes are necessarily accompanied by digestion of the provisional matrix. Allowing its replacement by normal basement membranes, made of type IV collagen, laminin, and nidogen. All of these events would lead in the most favorable case to restoration of the normal alveolo-capillary barrier. Low level MMP expression mediates normal matrix remodeling, while during inflammation and injury, large amounts of MMPs are produced presumably to repair damaged ECM
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