Associate Professor of Bioengineering and Airway Biology
My research focuses on the interface of mechanics and biology in the lung. We are interested in how lung cells respond to their mechanical environment, and how in turn they modify the lung’s mechanical behavior. Our motivation comes from chronic environmental lung diseases like asthma and pulmonary fibrosis, which are characterized by tissue remodeling that can be both irreversible and relentlessly progressive. We hypothesize that pathogenetic mechanisms unique to asthma and pulmonary fibrosis are inextricably linked to changes in the mechanical environment. Current efforts in the lab are focused on:
- Understanding the molecular mechanisms by which changes in the mechanical environment are transduced into biochemical signals in airway epithelium and lung fibroblasts.
- Identifying the network of genes regulated by the mechanical environment in airway epithelium and lung fibroblasts using high throughput gene arrays and bioinformatic analyses.
- Investigating the molecular pathways leading to, and the functional consequences of, epithelial (mucus metaplasia) and matrix remodeling.
The ultimate goal of these studies is to better understand the pathophysiology of asthma and pulmonary fibrosis within integrative frameworks that span the molecular to the tissue level, leading to novel preventive and therapeutic approaches to lung disease.
Tschumperlin, D.J., G. Dai, I.V. Maly, T. Kikuchi, L.H. Laiho, A.K. McVittie, K.J. Haley, C.M. Lilly, P.T.C. So, D.A. Lauffenburger, R.D. Kamm, J.M. Drazen. Mechanotransduction through growth-factor shedding into the extracellular space. Nature 429:83-6, 2004.
Leung, L.Y., D. Tian, C. P. Brangwynne, D.A. Weitz, D.J. Tschumperlin. A new microrheometry approach reveals individual and cooperative roles for TGF-beta1 and IL-1beta in fibroblast mediated stiffening of collagen gels. FASEB J. 21: 2064-73 , 2007.
Kojic, N., E. Chung, A.T. Kho, J. Park, A. Huang, P.T. So, D.J. Tschumperlin. An EGFR autocrine loop encodes a slow-reacting but dominant mode of mechanotransduction in a polarized epithelium. FASEB J. 24:1604-15, 2010.
Liu, F., J.D. Mih, B.S. Shea, A. Kho, A.S. Sharif, A.M. Tager, D.J. Tschumperlin. Feedback amplification of fibrosis through matrix stiffening and COX-2 suppression. J. Cell Biol. 190:693-706, 2010.
The Airway Mechanobiology Lab – The Tschumperlin and Drazen laboratory website
Ph.D., 1998, University of Pennsylvania