Contact Us

Mailing address:
Department of Environmental and Molecular Toxicology
Box 7633, NC State University
Raleigh, NC 27695-7633

Shipping address:
Suite 1104, 850 Main Campus Dr.
Raleigh, NC 27606

Phone 919.515.2274
Fax 919.515.7169

Alexia Taylor
Research Technician

Phil Bost
Graduate Student

Ellen Glista
Graduate Student

Brian Sayers
Graduate Student

James C. Bonner, Ph.D.
Associate Professor, Department of Environmental and Molecular Toxicology

Phone: 919-515-8615
E-mail: james_bonner@ncsu.edu

Education

BS, MS, Middle Tennessee State University
PhD, Mississippi State University
Postdoctoral, National Institute of Environmental Health Sciences

J. C. Bonner's CV

Research Interests

Pulmonary fibrosis encompasses several fatal environmental and occupational lung diseases for which there is currently no effective treatment strategy. More subtle fibrotic reactions also contribute to chronic airway remodeling observed in individuals with asthma, bronchitis, and chronic obstructive pulmonary disease (COPD). A common theme in the progression of fibrosis is the emergence of fibroblasts, connective tissue cells which proliferate and deposit collagen to define the fibrotic lesion.

Our laboratory studies the cellular and molecular mechanisms through which toxic environmental agents such as particles, nanoparticles, and metals cause fibroblast growth or matrix production resulting in fibrosis. Using a variety of molecular techniques, genomics and transgenic mouse models we have identified intracellular signaling pathways and novel genes that contribute to the progression of fibrosis. Our research has focused mainly on two families of cell surface growth factor receptor tyrosine kinases (RTK) that mediate these cellular responses: the platelet-derived growth factor receptor family (PDGFR) and the epidermal growth factor receptor family (EGFR). We have identified these RTKs as potentially important targets for therapeutic intervention of pulmonary fibrosis.

The emerging field of nanotechnology has prompted new initiatives aimed at understanding the possible health effects of manufactured nanomaterials (carbon nanotubes and nano-sized metal catalysts). Our goal is to determine the physico-chemical properties of nanomaterials that trigger fibrotic reactions in the lung in order to provide information for the design of safer nanomaterials. Of particular interest is determining the fibrotic potential of nanomaterials in mouse models of pre-existing lung disease such as asthma, viral infection, and bacterial endotoxin-induced inflammation.

“Are carbon nanotubes the next asbestos?” Visit the North Carolina Museum of Life and Science website and see the video to learn more: http://ncmls.org/learn-about/science-in-triangle/carbon-nanotubes

Bonner's Publications (PubMed)

Selected Publications

• Ryman-Rasmussen, J.P., M.F. Cesta, A.R. Brody, J.K. Shipley-Phillips, J.I. Everitt, E.W. Tewksbury, O.R. Moss, B.A. Wong, D.E. Dodd, M.E. Andersen, and J.C. Bonner. (2009) Inhaled carbon nanotubes reach the subpleural tissue in mice. Nature Nanotechnol. Nov;4(11):747-51. Epub 2009 Oct 25.



• Cesta, M.F., J.P. Ryman-Rasmussen, D.G. Wallace, T. Masinde, G. Hurlburt, A.J. Taylor, and J.C. Bonner. (2009) Bacterial Lipopolysaccharide Enhances PDGF Signaling and Pulmonary Fibrosis in Rats Exposed to Carbon Nanotubes. Am J Respir Cell Mol Biol. 2009 Sep 8. [Epub ahead of print]



• Bonner JC, Card JW, Zeldin DC. Nanoparticle-Mediated Drug Delivery and Pulmonary Hypertension. 2009 Mar 23. Hypertension [Epub ahead of print]



• Ryman-Rasmussen, J.P., E.W. Tewksbury, O.R. Moss, M.F. Cesta, B.A. Wong, and J.C. Bonner. (2009) Inhaled multiwalled carbon nanotubes potentiate airway fibrosis in a murine model of allergic asthma. Am J Respir Cell Mol Biol.40: 349-358.



• Card, J.W., D.C. Zeldin, J.C. Bonner, and E.R. Nestmann. (2008) Pulmonary applications and toxicity of engineered nanoparticles. Am J Physiol Lung Cell Mol Physiol. 2008 Sep;295(3):L400-11.



• Antao-Menezes, A., E.A. Turpin, P.C. Bost, J.P. Ryman-Rasmussen, and J.C. Bonner . (2008) STAT-1 signaling in human lung fibroblasts is induced by vanadium pentoxide through an IFN-beta autocrine loop. J. Immunol. 180(6):4200-4207.



• Voltz, J.W., J.W. Card, M.A. Carey, L.M. Degraff, C.D. Ferguson, G.P. Flake, J.C. Bonner , K.S. Korach, and D.C. Zeldin. (2008) Male Sex Hormones Exacerbate Lung Function Impairment After Bleomycin-Induced Pulmonary Fibrosis. Am. J. Respir. Cell. Mol. Biol . [Epub ahead of print].



• Bonner, J.C. (2007) Lung fibrotic responses to particle exposure. Toxicol Pathol . 35(1):148-53.



• Ingram, J.I., A. Antao-Menezes, E.A. Turpin, D.G. Wallace, J.B. Mangum, L.J. Pluta, R.S. Thomas, and J.C. Bonner . (2007) Genomic analysis of human lung fibroblasts exposed to vanadium pentoxide to identify
  candidate genes for occupational bronchitis. Respir. Res. 8:34.



• Mangum, J.B., E.A. Turpin, A. Antao-Menezes, M.F. Cesta, E. Bermudez, and J.C. Bonner (2006) Single-walled carbon nanotube (SWCNT)-induced interstital fibrosis in the lungs of rats is associated with increased PDGF mRNA and the formation of unique carbon structures that bridge alveolar macrophages in situ. Particle & Fibre Toxicol. 3:15.



• Ingram, J.I., A. Antao-Menezes, J.B. Mangum, O. Lyght, P.J. Lee, J.A. Elias, and J.C. Bonner. (2006) Opposing actions of Stat1 and Stat6 on IL-13-induced up-regulation of Egr-1 and PDGF ligands in pulmonary fibroblasts. J. Immunol. 177:4141-4148.



• Walters, D.M. J.L. Ingram, A.A. Menezes, A. Nyska, Y. Tani, S.R. Kleeberger, and J.C. Bonner. (2005) Susceptibility of STAT-1-deficient mice to pulmonary fibrogenesis. Am. J. Pathol. 167: 1221-9.



• Bonner, J. C. (2004). Regulation of PDGF and its receptors in fibrotic diseases. Cytokine Growth Factor Rev. 15, 255-273.



• Ingram, J. L., Rice, A. B., Geisenhoffer, K., Madtes, D. K., and Bonner, J. C. (2004). IL-13 and IL-1β promote lung fibroblast growth through coordinated up-regulation of PDGF-AA and PDGF-Rα. FASEB J. 18, 1132-1134.



• Ingram, J. L., Rice, A. B., Santos, J., Van Houten, B., and Bonner, J. C. (2003). Vanadium-induced HB-EGF expression in human lung fibroblasts is oxidant dependent and requires MAP kinases. Am. J. Physiol. 284, L774-L782.



• Osornio-Vargas, A. R., Bonner, J. C., Alfaro-Moreno, E., Martinez, L., Garcia-Cuellar, C., Ponce-de-Leon Rosales, S., Miranda, J., and Rosas, I. (2003). Proinflammatory and cytotoxic effects of Mexico City air pollution particulate matter in vitro are dependent on particle size and composition. Environ. Health Perspect. 111, 1289-1293.



• Wang, Y.-Z., Ingram, J. L., Walters, D. M., Rice, A. B., Santos, J. H., Van Houten, B., and Bonner, J. C. (2003). Vanadium-induced STAT-1 activation in lung myofibroblasts requires H2O2 and p38 MAP kinase. Free Radic. Biol. Med. 35, 845-855.



• Bonner, J. C., Rice, A. B., Ingram, J. L., Moomaw, C. R., Nyska, A., Bradbury A., Sessoms, A. R., Chulada, P. C., Morgan, D. L., Zeldin, D. C., and Langenbach, R. (2002). Susceptibility of cyclooxygenase-2-deficient mice to pulmonary fibrogenesis. Am. J. Pathol. 161, 459-470.



• Lindroos, P. M., Wang, Y.-Z., Rice, A. B., and Bonner, J. C. (2001). Regulation of PDGFR-alpha in rat pulmonary myofibroblasts by staurosporine. Am. J. Physiol. 280, L354-L362.



• Zhang, L., Rice, A. B., Adler, K., Sannes, P., Martin, L., Gladwell, W,, Koo, J. S., Gray, T. E., and Bonner, J. C. (2001). Vanadium stimulates human bronchial epithelial cells to produce heparin-binding epidermal growth factor-like growth factor: a mitogen for lung fibroblasts. Am. J. Respir. Cell. Mol. Biol. 24, 123-131.



• Bonner, J. C., Rice, A. B., Moomaw, C. R., and Morgan, D. L. (2000). Airway fibrosis in rats induced by vanadium pentoxide. Am. J. Physiol. 278, L209-L216.



• Wang, Y.-Z., Zhang, P., Rice, A. B., and Bonner, J. C. (2000). Regulation of interleukin-1ß-induced platelet-derived growth factor receptor-α expression in rat pulmonary myofibroblasts by p38 mitogen-activated protein kinase. J. Biol. Chem. 275, 22550-22557.



• Zhang, P., Wang, Y.-Z., Kagan, E., and Bonner, J. C. (2000). Peroxynitrite targets the epidermal growth factor receptor, Raf-1, and MEK independently to activate MAPK. J. Biol. Chem. 275, 22479-22486.