Respiratory Pharmacology Laboratory
Research
Current research focuses on the role of the peroxisome proliferator-activated receptor gamma (PPARgamma), a ligand-activated transcription factor, in the regulation of changes in lung structure and function that occur during the development of asthma and lung fibrosis. Recent publications from the group have established that the PPARgamma ligand, rosiglitazone inhibits cell proliferation and the release of mediators of inflammation from human airway smooth muscle cells (Ward et al., 2004). Significantly, rosiglitazone also reduces airways hyperresponsiveness in a mouse model of asthma (Ward et al., 2006). Current research exploring the mechanism of these actions in smooth muscle, fibroblasts and epithelial cells has been expanded through the synthesis of novel related drugs in collaboration with Dr Craig Hutton at the Bio21 Institute. A new project exploring the potential of airway cells to remodel the extracellular matrix, using an in vitro floating collagen gel model, shows significant promise to form the basis for an additional exciting new avenue of research.
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Key References
* WARD, J.E., FERNANDES, D.J., TAYLOR, C.C., BONACCI, J.V., QUAN, L. & STEWART, A.G. (2006) The PPARgamma ligand, rosiglitazone, reduces airways hyperresponsiveness in a murine model of allergen-induced inflammation. Pulmonary Pharmacology and Experimental Therapeutics, 19, 39-46.
* WARD, J.E., GOULD, H., HARRIS, T., BONACCI, J. & STEWART, A.G (2004). PPARgamma ligands 15-deoxy_delta12,14-prostaglandin J2 and rosiglitazone have different mechanisms for their anti-proliferative effects in human airway smooth muscle. Br. J. Pharmacol., 144, 517-525.
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