Dr. Ding's research focuses on cellular and extracellular environment interaction in various diseases and how such interactions affect the molecular mechanisms contributing to tissue injury and repair, as well as what drive these normal processes into deadly diseases. Dr. Ding's laboratory investigates the mechanisms by which multiple cell types and moleucalr signaling pathways regulate the development and outcome of lung fibrosis, lung injury, and even cancer progression. One of the projects is about focal adhesion kinase (FAK)-related non-kinase (FRNK). FAK plays an important role in regulation of fibroblast migration, differentiation, and proliferation, and cancer progression. Data from Dr. Ding's Laboratory have shown that FAK regulates cell proliferation through regulation of the expression of extracellular matrix proteins and Cyclin D1. The cytoplasmic protein FRNK acts to limit FAK-dependent cell migration and proliferation, as well as FAK mediated lung fibrosis, lung injury and cancer progression. For example, data from Dr. Ding's laboratory suggest that FRNK acts to limit myofibroblast differentiation induced by transforming growth factor beta-1 (TGF-beta-1), a core signaling process in the development of lung fibrosis. Another project in Dr. Ding's Laboratory is exploring the mechanism regulating the expression of FRNK, its signaling pathways, and how that signaling regulates the pro-fibrotic phenotype and plasticity of the cell types involved. Recently, the lab investigated post-transcriptional regulation and its role in pathogenesis, along with examining the therapeutic potentials of small molecular inhibitors of involved signaling pathways in treating pulmonary fibrosis, acute and chronic lung injury, cancer, cognitive dysfunction, and excessive tissue injury.
