James C Bonner

Summary

Affiliation: North Carolina State University
Country: USA

Publications

  1. doi request reprint Nickel nanoparticles cause exaggerated lung and airway remodeling in mice lacking the T-box transcription factor, TBX21 (T-bet)
    Ellen E Glista-Baker
    Environmental and Molecular Toxicology Program, Department of Biological Sciences, North Carolina State University, Campus Box 7633, Raleigh, North Carolina 27695, USA
    Part Fibre Toxicol 11:7. 2014
  2. pmc Multi-walled carbon nanotubes induce COX-2 and iNOS expression via MAP kinase-dependent and -independent mechanisms in mouse RAW264.7 macrophages
    Jong Kwon Lee
    Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, Research Triangle Park, Durham, NC 27709, USA
    Part Fibre Toxicol 9:14. 2012
  3. pmc Carbon nanotubes as delivery systems for respiratory disease: do the dangers outweigh the potential benefits?
    James C Bonner
    Department of Environmental and Molecular Toxicology, North Carolina State University, Raleigh, NC 27695, USA
    Expert Rev Respir Med 5:779-87. 2011
  4. pmc Mesenchymal cell survival in airway and interstitial pulmonary fibrosis
    James C Bonner
    Department of Environmental and Molecular Toxicology, North Carolina State University, Raleigh, North Carolina 27695, USA
    Fibrogenesis Tissue Repair 3:15. 2010
  5. pmc Nanoparticles as a potential cause of pleural and interstitial lung disease
    James C Bonner
    Department of Environmental and Molecular Toxicology, Campus Box 7633, Raleigh, NC 27695 7633, USA
    Proc Am Thorac Soc 7:138-41. 2010
  6. pmc Susceptibility of signal transducer and activator of transcription-1-deficient mice to pulmonary fibrogenesis
    Dianne M Walters
    CIIT Centers for Health Research, P O Box 12137, Research Triangle Park, NC 27709, USA
    Am J Pathol 167:1221-9. 2005
  7. ncbi request reprint Opposing actions of Stat1 and Stat6 on IL-13-induced up-regulation of early growth response-1 and platelet-derived growth factor ligands in pulmonary fibroblasts
    Jennifer L Ingram
    CIIT Centers for Health Research, Research Triangle Park, Durham, NC 27709, USA
    J Immunol 177:4141-8. 2006
  8. pmc Male sex hormones exacerbate lung function impairment after bleomycin-induced pulmonary fibrosis
    James W Voltz
    Division of Intramural Research, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA
    Am J Respir Cell Mol Biol 39:45-52. 2008
  9. ncbi request reprint Vanadium-induced STAT-1 activation in lung myofibroblasts requires H2O2 and P38 MAP kinase
    Yi Zhe Wang
    Laboratory of Pulmonary Pathobiology, National Institutes of Health, Research Triangle Park, NC 27709, USA
    Free Radic Biol Med 35:845-55. 2003
  10. ncbi request reprint IL-13 and IL-1beta promote lung fibroblast growth through coordinated up-regulation of PDGF-AA and PDGF-Ralpha
    Jennifer L Ingram
    National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, USA
    FASEB J 18:1132-4. 2004

Collaborators

Detail Information

Publications30

  1. doi request reprint Nickel nanoparticles cause exaggerated lung and airway remodeling in mice lacking the T-box transcription factor, TBX21 (T-bet)
    Ellen E Glista-Baker
    Environmental and Molecular Toxicology Program, Department of Biological Sciences, North Carolina State University, Campus Box 7633, Raleigh, North Carolina 27695, USA
    Part Fibre Toxicol 11:7. 2014
    ..The purpose of this study was to determine the role of T-bet in susceptibility to lung remodeling by NiNPs or MWCNTs...
  2. pmc Multi-walled carbon nanotubes induce COX-2 and iNOS expression via MAP kinase-dependent and -independent mechanisms in mouse RAW264.7 macrophages
    Jong Kwon Lee
    Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, Research Triangle Park, Durham, NC 27709, USA
    Part Fibre Toxicol 9:14. 2012
    ....
  3. pmc Carbon nanotubes as delivery systems for respiratory disease: do the dangers outweigh the potential benefits?
    James C Bonner
    Department of Environmental and Molecular Toxicology, North Carolina State University, Raleigh, NC 27695, USA
    Expert Rev Respir Med 5:779-87. 2011
    ..However, functionalization of CNTs to modulate aspect ratio, biodegradability and to remove residual metals could allow for safe design of CNTs for use in drug delivery in certain circumstances...
  4. pmc Mesenchymal cell survival in airway and interstitial pulmonary fibrosis
    James C Bonner
    Department of Environmental and Molecular Toxicology, North Carolina State University, Raleigh, North Carolina 27695, USA
    Fibrogenesis Tissue Repair 3:15. 2010
    ..Understanding the mechanisms that regulate the survival or death of mesenchymal cells is central to ultimately developing therapeutic strategies for lung fibrosis...
  5. pmc Nanoparticles as a potential cause of pleural and interstitial lung disease
    James C Bonner
    Department of Environmental and Molecular Toxicology, Campus Box 7633, Raleigh, NC 27695 7633, USA
    Proc Am Thorac Soc 7:138-41. 2010
    ....
  6. pmc Susceptibility of signal transducer and activator of transcription-1-deficient mice to pulmonary fibrogenesis
    Dianne M Walters
    CIIT Centers for Health Research, P O Box 12137, Research Triangle Park, NC 27709, USA
    Am J Pathol 167:1221-9. 2005
    ....
  7. ncbi request reprint Opposing actions of Stat1 and Stat6 on IL-13-induced up-regulation of early growth response-1 and platelet-derived growth factor ligands in pulmonary fibroblasts
    Jennifer L Ingram
    CIIT Centers for Health Research, Research Triangle Park, Durham, NC 27709, USA
    J Immunol 177:4141-8. 2006
    ..This novel mechanism could aid in identifying molecular targets for the treatment of chronic airway remodeling and fibrosis in asthma...
  8. pmc Male sex hormones exacerbate lung function impairment after bleomycin-induced pulmonary fibrosis
    James W Voltz
    Division of Intramural Research, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA
    Am J Respir Cell Mol Biol 39:45-52. 2008
    ..Sex differences should be carefully considered when designing and interpreting experimental models of pulmonary fibrosis in mice...
  9. ncbi request reprint Vanadium-induced STAT-1 activation in lung myofibroblasts requires H2O2 and P38 MAP kinase
    Yi Zhe Wang
    Laboratory of Pulmonary Pathobiology, National Institutes of Health, Research Triangle Park, NC 27709, USA
    Free Radic Biol Med 35:845-55. 2003
    ..Moreover, p38 MAPK and EGF receptor activation are required for V2O5-induced STAT-1 activation...
  10. ncbi request reprint IL-13 and IL-1beta promote lung fibroblast growth through coordinated up-regulation of PDGF-AA and PDGF-Ralpha
    Jennifer L Ingram
    National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, USA
    FASEB J 18:1132-4. 2004
    ..Our findings indicate that IL-13 acts in synergy with IL-1beta to stimulate growth by coordinately up-regulating PDGF-AA and the PDGF-Ralpha, respectively...
  11. ncbi request reprint Vanadium-induced HB-EGF expression in human lung fibroblasts is oxidant dependent and requires MAP kinases
    Jennifer L Ingram
    Laboratory of Pulmonary Pathobiology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA
    Am J Physiol Lung Cell Mol Physiol 284:L774-82. 2003
    ..The induction of HB-EGF is not related to a burst of H(2)O(2) in V(2)O(5) treated cells, yet the action of V(2)O(5) in upregulating HB-EGF is oxidant dependent and could be due to the reaction of V(2)O(5) with endogenous H(2)O(2)...
  12. pmc Cyclooxygenase-2 deficiency exacerbates bleomycin-induced lung dysfunction but not fibrosis
    Jeffrey W Card
    Division of Intramural Research, National Institute of Environmental Health Sciences, National Institutes of Health, NC 27709, USA
    Am J Respir Cell Mol Biol 37:300-8. 2007
    ..Collectively, these data suggest an important regulatory role for COX-2 in the maintenance of lung function in the setting of lung fibrosis, but not in the progression of the fibrotic process per se...
  13. ncbi request reprint STAT-1 signaling in human lung fibroblasts is induced by vanadium pentoxide through an IFN-beta autocrine loop
    Aurita Antao-Menezes
    Hamner Institutes for Health Sciences, Research Triangle Park, NC 27709, USA
    J Immunol 180:4200-7. 2008
    ..This mechanism is postulated to counterbalance profibrogenic mechanisms that follow V(2)O(5) injury...
  14. pmc Inhaled multiwalled carbon nanotubes potentiate airway fibrosis in murine allergic asthma
    Jessica P Ryman-Rasmussen
    North Carolina State University, Box 7633, Raleigh, NC 27695, USA
    Am J Respir Cell Mol Biol 40:349-58. 2009
    ..These data indicate that inhaled MWCNT require pre-existing inflammation to cause airway fibrosis. Our findings suggest that individuals with pre-existing allergic inflammation may be susceptible to airway fibrosis from inhaled MWCNT...
  15. pmc Respiratory syncytial virus infection reduces lung inflammation and fibrosis in mice exposed to vanadium pentoxide
    Elizabeth A Turpin
    The Hamner Institutes for Health Sciences, Research Triangle Park, North Carolina 27709, USA
    Respir Res 11:20. 2010
    ..It is unknown whether individuals with pre-existing respiratory viral infection are susceptible to V2O5-induced bronchitis. We hypothesized that respiratory viral infection will exacerbate vanadium-induced lung fibrosis...
  16. ncbi request reprint Regulation of PDGF and its receptors in fibrotic diseases
    James C Bonner
    National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA
    Cytokine Growth Factor Rev 15:255-73. 2004
    ..This review summarizes the literature on the role of PDGF and its receptors in the development of fibrosis in a variety of organ systems, including lung, liver, kidney, and skin...
  17. pmc Nickel nanoparticles enhance platelet-derived growth factor-induced chemokine expression by mesothelial cells via prolonged mitogen-activated protein kinase activation
    Ellen E Glista-Baker
    Department of Environmental and Molecular Toxicology, North Carolina State University, Raleigh, NC 27695 7633, USA
    Am J Respir Cell Mol Biol 47:552-61. 2012
    ..These data indicate that NiNPs enhance the activity of PDGF in regulating chemokine production in NRM2 cells through a mechanism involving reactive oxygen species generation and prolonged activation of ERK-1,2...
  18. ncbi request reprint Interleukin-13 stimulates the proliferation of lung myofibroblasts via a signal transducer and activator of transcription-6-dependent mechanism: a possible mechanism for the development of airway fibrosis in asthma
    Jennifer L Ingram
    Laboratory of Pulmonary Pathobiology Drs Ingram and Bonner, Ms Rice, and Ms Geisenhoffer, National Institute of Environmental Health Science, Research Triangle Park, NC 27709, USA
    Chest 123:422S-4S. 2003
  19. pmc Genomic analysis of human lung fibroblasts exposed to vanadium pentoxide to identify candidate genes for occupational bronchitis
    Jennifer L Ingram
    The Hamner Institutes for Health Sciences, Research Triangle Park, North Carolina 27709, USA
    Respir Res 8:34. 2007
    ....
  20. pmc Role of cyclooxygenase-2 in exacerbation of allergen-induced airway remodeling by multiwalled carbon nanotubes
    Brian C Sayers
    1 Department of Environmental and Molecular Toxicology, North Carolina State University, Raleigh, North Carolina
    Am J Respir Cell Mol Biol 49:525-35. 2013
    ..We conclude that exacerbations of allergen-induced airway inflammation and mucus-cell metaplasia by MWCNTs are enhanced by deficiencies in COX-2, and are associated with the activation of a mixed Th1/Th2/Th17 immune response...
  21. pmc Bacterial lipopolysaccharide enhances PDGF signaling and pulmonary fibrosis in rats exposed to carbon nanotubes
    Mark F Cesta
    Department of Environmental and Molecular Toxicology, North Carolina State University, Raleigh, 27695 7633, USA
    Am J Respir Cell Mol Biol 43:142-51. 2010
    ..Our findings also suggest that individuals with pre-existing pulmonary inflammation are at greater risk for the potential adverse effects of MWCNT...
  22. ncbi request reprint Lung fibrotic responses to particle exposure
    James C Bonner
    Respiratory Biology Program, Division of Biological Sciences, CIIT Centers for Health Research, Research Triangle Park, NC 27709, USA
    Toxicol Pathol 35:148-53. 2007
    ....
  23. ncbi request reprint ErbB2 activity is required for airway epithelial repair following neutrophil elastase exposure
    Bernard M Fischer
    Department of Pediatrics, Duke University Medical Center, Durham, North Carolina 27710, USA
    FASEB J 19:1374-6. 2005
    ..1 microM), an ErbB2-neutralizing antibody, blocked thymidine incorporation only in NE-treated cells. These results suggest ErbB2 is a critical factor for epithelial recovery following NE exposure...
  24. pmc Over-expression of human endosulfatase-1 exacerbates cadmium-induced injury to transformed human lung cells in vitro
    Huiying Zhang
    Department of Molecular Biomedical Sciences, Center for Comparative Molecular Translational Research, College of Veterinary Medicine, NC State University, Raleigh, NC 27607, USA
    Toxicol Appl Pharmacol 265:27-42. 2012
    ....
  25. pmc Interlaboratory evaluation of rodent pulmonary responses to engineered nanomaterials: the NIEHS Nano GO Consortium
    James C Bonner
    Department of Environmental and Molecular Toxicology, North Carolina State University, Raleigh, North Carolina, USA
    Environ Health Perspect 121:676-82. 2013
    ..Engineered nanomaterials (ENMs) have potential benefits, but they also present safety concerns for human health. Interlaboratory studies in rodents using standardized protocols are needed to assess ENM toxicity...
  26. ncbi request reprint p38 mitogen-activated protein kinase regulates growth factor-induced mitogenesis of rat pulmonary myofibroblasts
    Annette B Rice
    Airway Inflammation Group, Laboratory of Pulmonary Pathobiology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, USA
    Am J Respir Cell Mol Biol 27:759-65. 2002
    ..Collectively, these data demonstrate that p38 MAP kinase activation negatively regulates PDGF- and EGF-mediated growth responses by directly interacting with ERK1/2 and suppressing its phosphorylation...
  27. ncbi request reprint EGF and PDGF receptor tyrosine kinases as therapeutic targets for chronic lung diseases
    Jennifer L Ingram
    Division of Pulmonary, Allergy and Critical Care Medicine, Duke University Medical Center, Durham, North Carolina 27709, USA
    Curr Mol Med 6:409-21. 2006
    ..A full understanding of the complex mechanisms involving these receptors and ligands should lead to therapeutic strategies for the treatment of a wide range of fibroproliferative lung diseases...
  28. pmc Inhaled carbon nanotubes reach the subpleural tissue in mice
    Jessica P Ryman-Rasmussen
    Department of Environmental and Molecular Toxicology, College of Agricultural and Life Sciences, North Carolina State University, Raleigh, NC 27695, USA
    Nat Nanotechnol 4:747-51. 2009
    ..This work suggests that minimizing inhalation of nanotubes during handling is prudent until further long-term assessments are conducted...
  29. ncbi request reprint Proliferation of the airway epithelium in asthma: are inflammatory cells required?
    Brian W Booth
    North Carolina State University, Raleigh, NC 27606, USA
    Chest 123:384S-5S. 2003
  30. pmc Susceptibility of cyclooxygenase-2-deficient mice to pulmonary fibrogenesis
    James C Bonner
    Laboratory of Pulmonary Pathobiology, National Institute of Environmental Health Sciences, National Institute of Health, Research Triangle Park, North Carolina 27709, USA
    Am J Pathol 161:459-70. 2002
    ..These findings indicate that the COX-2 enzyme is protective against pulmonary fibrogenesis, and we suggest that COX-2 generation of PGE(2) is an important factor in resolving inflammation...