Bridges Laboratory
My primary research interests are focused toward: 1) understanding the regulation of alveolar epithelial cell maturation during lung development and 2) determining the molecular regulation of surfactant pool sizes in the postnatal and adult lung, with particular interest in diseases associated with surfactant dysfunction. My graduate work focused on the cellular and pathophysiological consequences of disease-linked mutations in the surfactant protein C gene using cell-based assays and transgenic mice. Subsequent postdoctoral studies as a Parker B. Francis pulmonary fellow investigated the function and regulation of the acyltransferase LPCAT1 in the production of saturated phosphatidylcholine (SatPC) in alveolar epithelial type II (AT2) cells, and the role of hypoxia inducible factors during lung development. I continue to pursue these areas of interest, including investigating the mechanisms of pulmonary alveolar proteinosis with respect to GPR116 signaling in AT2 cells and ABCA3-mediated interstitial lung disease in children, as well as bolster projects centered on the transcriptional control of alveolar epithelial cell regeneration during lung repair. In addition, we have recently identified a novel adeno-associated virus (AAV) serotype that targets AT2 cells in vivo with high efficiency and specificity. My laboratory is well poised to assist in determining the role of IGSF3 in AT2 cell barrier function. My laboratory has been isolating, culturing, and functionally characterizing primary AT2 cells from various transgenic mouse models for over 15 years and have recently optimized culture techniques to generate highly differentiated human 2D monolayer and 3D alveolar organoids. We have also optimized transduction of primary AT2 cells in culture to knockdown or overexpress genes of interest using AAV approaches.
Lab Resources and Services
The Bridges Lab is located in the Division of Pulmonary, Critical Care & Sleep Medicine, within the Department of Medicine
Current Projects
James P. Bridges, PhD