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Gary Hoyle, PhD

Environmental and Occupational Health Sciences

Role: Faculty
Title: Professor
Office No: Research Tower, Room 701, Health Science Center
Address: 3319 Abraham Flexner Way, Louisville, KY 40202
Lab No: Research Tower, Room 702
Phone: 502/852-7337
Fax: 502/852-7889


Gary W. Hoyle will join the University of Louisville School of Public Health and Information Sciences as a professor in the Department of Environmental and Occupational Health Sciences and University Scholar on August 1, 2007. 

Dr. Hoyle was previously a faculty member in Tulane University’s Department of Medicine, Section of Pulmonary Disease, Critical Care and Environmental Medicine. 

Dr. Hoyle’s research interests focus on mechanisms of lung injury and inflammation, including the regulation of lung injury and repair by G proteins, the role of sensory nerves and nerve growth factor in environmental and occupational lung disease, and the control of DNA damage and repair by sensory neuropeptide receptors.

He has more than 12 years of uninterrupted extramural federal funding from the National Institutes of Health (NIH), U.S. Environmental Protection Agency (EPA) and the Department of Defense.  He was recently awarded a $1.3M grant from the NIH to study novel therapies for chlorine gas exposure.  This research will continue at the University of Louisville. 

Dr. Hoyle received his B.A. from Johns Hopkins University, his Ph.D. in Biochemistry from Duke University, and completed post-doctoral fellowship training at the University of Pennsylvania.

Research Interests

Mechanisms of lung injury and inflammation
G protein signaling
Sensory nerves and inflammation
Air pollution and asthma
Nerve growth factor and airway disease

Current Projects

1. Novel therapies for chlorine-induced lung injury.  NIH/NIEHS U01 ES015673.  Principal Investigator, 9/29/06-5/31/11.

2. Levalbuterol and acute lung injury.  Sepracor, Inc.  Principal Investigator, 12/7/07-12/6/08.

3. Neuroanatomy and molecular biology of airway neurons.  R01 HL035812. Co-investigator (Richard Dey, Principal Investigator), 4/1/07-3/31/12.

4. Role of EBV gene products in the pathogenesis of IPF.  NIH/NHLBI R01 HL083901.  Co-investigator (Joseph Lasky, Principal Investigator), 5/1/06-4/30/10.

5. Nerve growth factor and asthma.

Recent Publications

Lee, C.-T., Poovey, H. G., Rando, R. J., Friedman, M., and Hoyle, G. W.  (2003).  An HDI polyisocyanate aerosol exposure system for large-scale animal experiments.  Am. Ind. Hyg. Assoc. J. 64:439-444.

Lee, C.-T., Friedman, M., Poovey, H. G., Ie, S. R., Rando, R. J., and Hoyle, G. W.  (2003).  Pulmonary toxicity of hexamethylene diisocyanate aerosols in mice.  Toxicol. Appl. Pharmacol. 188:154-164.

Zhuo, Y., Hoyle G. W., Zhang, J., Morris, G., and Lasky, J. A.  (2003).  A novel murine PDGF-D splicing variant results in significant differences in peptide expression and function.  Biochem. Biophys. Res. Commun. 308:126-132.

Hoyle, G. W.  (2003).  Neurotrophins and lung disease.  Cytokine Growth Factor Rev. 14:551-558.

Vuillemenot, B. R., Rodriguez, J. F., and Hoyle, G. W.  (2004).  Lymphoid tissue and emphysema in the lungs of transgenic mice inducibly expressing TNF-.  Am. J. Resp. Cell Mol. Biol. 30:438-448.

Henson, M. C., Swan, K. F., Edwards, D. E., Hoyle, G. W., Purcell, J., and Castracane, V. D.  Leptin receptor expression in fetal lung is enhanced in late gestation in the baboon: a model for human pregnancy.  (2004).  Reproduction 127:87-94.

Quarcoo, D., Schulte-Herbruggen, O., Lommatzsch, M., Schierhorn, K., Hoyle, G. W., Renz, H., and Braun, A.  (2004).  Nerve growth factor induces increased airway inflammation via a neuropeptide-dependent mechanism in a transgenic animal model of allergic airway inflammation.  Clin. Exp. Allergy 34:1146-1151.

Curiel, T. J., Cheng, P., Mottram, P., Alvarez, X., Moons, L., Evdemon-Hogan, M., Wei, .S, Zou, L., Kryczek, I., Hoyle, G., Lackner, A., Carmeliet, and P., Zou, W.  (2004).  Dendritic cell subsets differentially regulate angiogenesis in human ovarian cancer.  Cancer Res. 64:5535-5538.

Li, J., Poovey, H. G., Rodriguez, J. F., Brody, A. R., and Hoyle, G. W.  (2004).  Effect of platelet-derived growth factor on the development and persistence of asbestos-induced fibroproliferative lung disease.  J. Environ. Path. Toxicol. Oncol. 23:253-266.

Lee, C.-T., Ylostalo, J., Friedman, M., and Hoyle, G. W.  (2005).  Gene expression profiling in mouse lung following polymeric hexamethylene diisocyanate exposure.  Toxicol. Appl. Pharmacol. 205:53-64.

Zhou, Y., Hoyle, G. W., and Lasky, J. A.  (2006).  Overexpression of PDGF-C using a lung-specific promoter results in abnormal lung development.  Transgenic Res. 15:543-555.

Grad, I., McKee, T. A., Ludwig, S. M., Hoyle, G. W., Ruiz, P., Wurst, W., Floss, T., Miller, C. A., III, and Picard., D.  (2006).  The Hsp90 co-chaperone p23 is essential for perinatal survival.  Mol. Cell. Biol. 26:8976-8983.

Williams, R., Zou, Y., and Hoyle, G. W.  (2007).  The tachykinin 1 receptor activates NF-B in lung epithelial cells through a Gq-dependent pathway.  Am. J. Physiol. Lung Cell. Mol. Physiol. 292:L430-L437.

Zwezdaryk, K. J., Coffelt, S. B., Figueroa, Y. G., Liu, J., Phinney, D. G., LaMarca, H. L., Florez, L., Morris, C. B., Hoyle, G. W., and Scandurro, A. B.  (2007).  Erythropoietin, a hypoxia-regulated factor, elicits a pro-angiogenic program in human mesenchymal cells.  Exp. Hematol. 35:640-652.

Lee, C.-T., Poovey, H. G., Rando, R. J., and Hoyle, G. W.  (2007).  Neuronal modulation of lung injury induced by polymeric hexamethylene diisocyanate in mice.  Toxicol. Appl. Pharmacol. 224, 19-28.

Fattman, C., Gambelli, F., Hoyle, G., Pitt, B., and Ortiz, L.  (2008).  Epithelial expression of TIMP1 does not alter sensitivity to bleomycin-induced lung injuriy in C57BL/6 mice.  Am. J. Physiol. Lung Cell. Mol. Physiol. doi:10.1152/ajplung.00291.2007.

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