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The common endpoints of lung injury are emphysema, in which airspaces become enlarged but their walls show minor changes, and pulmonary fibrosis, in which the airspace walls are scarred and airspaces are lost. Over the years, our lab has been interested in establishing the mechanisms leading to these divergent responses. Currently, we are exploring the processes which enable fibroblasts to leave the alveolar walls and invade airspaces, one of the key processes leading to lung dysfunction in pulmonary fibrosis. A group of biochemically dissimilar proteins share the functional property of decreasing cell adhesion to extracellular matrix, stimulating cell migration and replication and (in some cases) altering gene expression. We are investigating the involvement of these proteins using a combination of animal models and studies of biopsies as available. An animal model of unilateral matrix synthesis from extracellular matrix synthesis in a context of inflammation and fibroblast migration.
Kuhn, C., Pathology of pulmonary fibrosis. In: Pulmonary Fibrosis, S. Phan and R. Thrall (eds.), New York, Marcel Dekker, pp59-82, 1995. Kuhn, C., & Mason, R.J. The immunolocalization of SPARC, tenascin, thrombospondin in pulmonary fibrosis. Am. J. Pathol. 147:1759-1769, 1995. |
 Professor M.D., Washington University, 1959 Memorial Hospital of Rhode Island Hodgson, H150 729-2393 FAX 729-3204 |