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

 

Lexie

Alexia Taylor
Research Technician

 

Phil

Phil Bost
Graduate Student

 

Ellen

Ellen Glista
Graduate Student

 

Brian

Brian Sayers
Graduate Student

JamieJames 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.

 

 

Bonner

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

  • 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.

 

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