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The major focus of my research is to identify cellular and molecular mechanisms by which G protein-coupled receptors (GPCRs) mediate important functions in airway cells. GPCR signaling regulates contractile function, synthesis and release of autocrine factors, and cell growth/survival in various airway cells, including airway smooth muscle (ASM), airway epithelium, lung fibroblasts, and T lymphocytes. Aberrant GPCR signaling or exaggerated presentation of GPCR stimuli can promote ASM hypercontractility, airway remodeling, and ASM hyperplasia/hypertrophy, all of which contribute to the pathogenesis of asthma and COPD. Moreover, GPCRs appear to mediate important mitogenic and survival signaling pathways in cells comprising the tumor microenvironment- including epithelia, fibroblasts, stem cells, and inflammatory cells- rendering them potentially important therapeutic targets in the treatment of cancer. Finally, many GPCR genes possess mutations that alter their expression or function; we are particularly interested in characterizing such altered function and its contribution to disease state or disease therapy.



  • Identify OGR1 as the principal proton-sensing receptor in the airway, capable of regulating airway resistance via its function of airway smooth muscle.
  • Identify inflammation, and microaspiration of acid, as two mediators of low pH in the airway lumen.
  • List 2 specific drugs that can function as OGR1 activators and potential asthma therapeutics.

Presentation: PowerPoint slides only, no audio