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Lynn
M. Schnapp, M.D.
Professor of Medicine
Pulmonary and Critical Care Medicine
OFFICE ADDRESS
Center for Lung Biology
815 Mercer Bldg., Rm S349
Campus Box 358052
Seattle, WA 98109
lschnapp@u.washington.edu
Academic Office: (206) 897-5389
Fax: (206) 897-5390
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EDUCATION AND TRAINING
B.S., Massachusetts Institute of Technology
Cambridge, MA, 1978-1982.
M.D., University of Pennsylvania, Philadelphia,
PA, 1982-1986.
Residency in Internal Medicine, Hospital of the
University of Pennsylvania, Philadelphia, PA,
1986-1989.
Fellowship in Pulmonary and Critical Care
Medicine, University of California, San
Francisco, San Francisco, CA, 1989-1992.
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CURRENT
RESEARCH INTERESTS
Mechanisms of Acute Lung Injury and Repair
Our lab is focused on the processes that govern acute lung injury and its resolution. In particular, we are interested in matrix remodeling and why lung injury resolves under certain circumstances (i.e. Adult Respiratory Distress Syndrome) and progresses to end-stage fibrosis in other circumstances (i.e. Idiopathic Pulmonary Fibrosis). To examine these questions, we use different mouse models of lung injury to examine the regulation of matrix remodeling and the role of the alveolar myofibroblasts in the resolution of fibrosis. To complement these studies, we are analyzing bronchoalveolar lavage fluid from patients with acute lung injury and other lung diseases using cutting-edge methodologies in proteomics to identify new pathways in lung injury. We also are studying pathways that regulate lymphocyte trafficking to the lung during inflammation and injury.
Another focus in the laboratory is to characterize the interactions of the extracellular environment with HIV in the lung. The lung is an important reservoir of HIV and site of HIV replication, which results in virus-induced lung injury. How HIV leads to direct lung injury, and how virus replication is sustained within the lung, are not known. We hypothesize that extracellular matrix (ECM) enhance and sustain IV infection within the lung and, conversely, that HIV within the lung alters ECM and contributes to inflammation and fibrosis.
REPRESENTATIVE PUBLICATIONS
Farias E, Lu M, Li X, Schnapp LM. The integrin alpha 8 beta 1-fibronectin mediates cell survival via PI3 kinase pathway. Biochem Biophys Res Commun. 329(1):305-11 2005.
Schnapp LM Donohue S, Chen JZ, Sunde DA, Kelly PM, Ruzinski J, Martin TR, Goodlet DR. Mining the ARDS proteome: identification of IGF/IGFBP-3 pathway in lung injury. Am J Pathol. 169:86-95 2006
Li L, Schwartz B, Tsubota Y, Raines E, Kiyokawa H, Yonekawa K, Harlan JM, Schnapp LM. Cyclin-dependent kinase inhibitors block leukocyte adhesion and migration. J Immunol. 180(3):1808-17, 2008
Chen JZ Ryu S, Gharib S, Goodlett DR, Schnapp LM. Exploration of the Normal Human BALF Proteome. Proteomics: Clinical Applications. 2(4) 585-595, 2008
Smith L, Wagner TE, Huizar H, Schnapp LM. Expression of the Collagen Receptor uPARAP During Murine Lung Development. Gene Expression Patterns, 8:486-93, 2008
Choi, J, Lee SS, Sunde, D, Huizar H, Haugk K, Thannickal V, Vittal R, Plymate S, Schnapp LM. Blockade of Insulin-like Growth Factor 1 pathway in mouse model of lung injury and fibrosis improves outcome. Am J Respir Crit Care Med. In Press, 2008 |
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Last Updated:
July 2, 2009
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