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(American Journal of Pathology. 2000;156:1927-1935.)
© 2000 American Society for Investigative Pathology

Regular Articles

Expression of the Integrin {alpha}8ß1 during Pulmonary and Hepatic Fibrosis

David Levine*, Don C. Rockey{dagger}, Teresa A. Milner{ddagger}, Johannes M. Breuss§, John T. Fallon and Lynn M. Schnapp*

From the Division of Pulmonary and Critical Care Medicine,*
Department of Medicine, Mount Sinai School of Medicine, New York, New York; the Division of Gastroenterology,{dagger}
Duke University Medical Center, Durham, North Carolina; the Department of Neurology and Neuroscience,{ddagger}
Weill Medical College of Cornell, New York, New York; the Institute for Vascular Biology and Thrombosis Research,§
University of Vienna, Vienna, Austria; and the Cardiovascular Institute,
Departments of Medicine and Pathology, Mount Sinai School of Medicine, New York, New York

The fibrotic response after diverse forms of injury is characterized by the accumulation of extracellular matrix proteins, proliferation of myofibroblast-like cells, and organ contraction. Myofibroblasts are key effector cells in the development of the fibrotic response. They contribute to fibrosis through both increased cell number (proliferation) and enhanced matrix synthesis. Integrins, a class of cell adhesion molecules, are mediators of cell-extracellular matrix protein interactions that are important in the proliferative and migratory response of cells to matrix proteins. We have previously cloned the human integrin subunit {alpha}8, documented its high expression in lung tissue, and established it as a receptor for the matrix proteins fibronectin, vitronectin, and tenascin. We now demonstrate that alveolar interstitial cells are the primary cell type expressing {alpha}8ß1 in the lung parenchyma. Expression of {alpha}8ß1 is concentrated primarily along the thinned extensions of cells and at the tips of filopodia. Because of its unique distribution in alveolar interstitial cells, we hypothesized that it may play a role in the fibrotic response after injury. In bleomycin-induced pulmonary fibrosis, there is increased expression of {alpha}8ß1 by interstitial fibroblasts, the majority of which coexpress {alpha} smooth muscle actin, a marker of tissue myofibroblasts. To establish a more general role for {alpha}8ß1 during organ fibrosis, we further examined its expression in two rat models of liver fibrosis. During hepatic injury due to either carbon tetrachloride injury or bile duct ligation, we demonstrate de novo expression of {alpha}8ß1 in activated hepatic stellate cells, the myofibroblast equivalent in liver. Taken together, the data localize {alpha}8ß1 to myofibroblast-like cells during wound healing and suggest that signal transduction through the {alpha}8ß1 integrin may contribute to the fibrotic response of organs to injury.




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