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Transcript
Regulation of Lung Ion Transport
Faculty: O’Grady, Ingbar
This theme developed from our original NIH SCOR in Acute Lung Injury addressing the
molecular basis of ion transport in lung epithelial cells and lung alveolar solute and solvent flux
during lung development and after lung injury; and the biochemical regulation of transport
proteins. Dr Doug Wangsteen, Professor of Physiology, assists in measurements of transport in
intact lungs and in living animals.
David Ingbar, M.D. Professor of Medicine, Pediatrics and Integrative Biology & Physiology
Molecular Regulation of Alveolar Epithelial Ion Transport & Function: We study the
regulation of alveolar epithelial function during lung development, injury and repair. Most
studies focus on Na,K-ATPase and other ion transport proteins, with additional interest in
epithelial migration, matrix interactions, and apoptosis. A major goal is to develop therapeutic
strategies to upregulate: (i) sodium pump function and/or (ii) cell migration to reform the
epithelial barrier and increase alveolar fluid resorption. Current studies utilize hormones
(glucocorticoids, T3), to stimulate Na,K-ATPase in vitro and in vivo. We also examine the type II
cell response to hypoxia and hyperoxia at the translatome and transcriptome levels. With Dr.
O’Grady, we found that CFTR Cl channel is required for beta agonist stimulation of alveolar fluid
clearance.
Scott O’Grady, Ph.D., Professor of Animal Science and Integrative Biology & Physiology
Epithelial Ion Transport Mechanisms: My laboratory seeks to understand the basic
mechanisms of transepithelial ion transport. We utilize several electrophysiological techniques
(including patch clamp, two electrode voltage clamp, epithelial voltage clamp), imaging
technology and molecular approaches to investigate mechanisms and regulation of electrolyte
transport across airway and alveolar epithelial cells. We also study aspects of innate immune
function of the airway epithelium related to allergic responses to enviornmental allergens and
the pathogenesis of asthma.