Pulmonary Fibrosis and Lung Scarring

Lung scarring, or pulmonary fibrosis is a devastating disease with poor prognosis. We are particularly interested in Idiopathic Pulmonary Fibrosis, which is a scarring disease of unknown origin. One of the hallmarks of pulmonary fibrosis is the accumulation of scar forming myofibroblasts, which differentiate from lung fibroblasts during fibrosis. Myofibroblasts secrete extracellular matrix proteins such as collagen, which leads to scarring. Our lab studies the molecular mechanisms surrounding the differentiation of fibroblasts into myofibroblasts. We also study differences in lung fibroblasts isolated from patients with Idiopathic Pulmonary Fibrosis and fibroblasts isolated from healthy lung tissues. The current fibrosis related projects in the lab are focused on how pro-fibrotic cytokines such as TGFbeta negatively regulate a family of proton-sensing GPCRs including the ovarian cancer G-protein receptor 1 (OGR1) and the T-cell death associated gene 8 (TDAG8) and how TGFbeta induced downregulation of OGR1 and TDAG8 may induce pulmonary fibrosis. A parallel project focuses on the anti-fibrotic properties of ligands for these receptors. These projects utilize primary human lung fibroblasts and in vivo animal models of fibrosis which include radiation, silica dust, and bleomycin induced lung scarring. Techniques and areas of investigation: primary fibroblast isolation from patients, cell culture, preclinical animal models, cell biology, flow cytometry, ELISA, qRT-PCR, western blot, immunofluorescence and immunohistochemical staining.

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