Jacob N. Finkelstein, Ph.D.

Dr. Finkelstein's laboratory research emphasizes the role of the alveolar epithelium in modulating the pulmonary injury response to physiological and toxicological stimuli. This includes studies of oxidant induced signaling in the pulmonary epithelium and macrophages and epithelial production of cytokines and chemokines in the regulation of the inflammatory functions of alveolar macrophages. His previous research effort focused on the pulmonary alveolar type II cell as the site of pulmonary surfactant synthesis and secretion, and studies on the basic cell and molecular biology of these processes are still an important facet of his work. In addition, the type II cell also plays an important role as the stem cell for renewal of the alveolar epithelium both in the normal lung development and during epithelial repair and renewal following lung injury. The most recent data suggest that type II cells may also be involved in regulating the inflammatory functions of alveolar macrophages, as well as the actions of interstitial fibroblasts during lung growth or pulmonary fibrosis.
The overall goal of the current research is to identify some of the key control mechanisms involved in epithelial cell and fibroblast proliferation, and in related extracellular matrix synthesis, processing and assembly. This work seeks to define such mechanisms not only during normal lung growth and normal development, but also during the repair of epithelial damage, and may have important implications for pediatric and adult lung disease, including bronchopulmonary dysplasia (BPD) in premature infants. This work is funded by grants from NIH, EPA and DoD.

The overall goal of some of their additional current research is to identify some of the key control mechanisms involved in epithelial cell and fibroblast proliferation, and in related extracellular matrix synthesis, processing and assembly. This work seeks to define such mechanisms not only during normal lung growth and normal development, but also during the repair of epithelial damage, and may have important implications for pediatric and adult lung disease, including bronchopulmonary dysplasia (BPD) in premature infants.