Research Topics
Genomes and Genes | James C BonnerSummaryAffiliation: National Institutes of Health Country: USA Publications
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Detail Information
Publications
Induction of the lung myofibroblast PDGF receptor system by urban ambient particles from Mexico CityJ C Bonner
Airway Inflammation Section, Laboratory of Pulmonary Pathobiology, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA
Am J Respir Cell Mol Biol 19:672-80. 1998..These findings suggest that PM10 particles induce expression of the PDGF receptor system through macrophage-dependent and -independent mechanisms involving endotoxin and metals...- Airway fibrosis in rats induced by vanadium pentoxideJ C Bonner
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 278:L209-16. 2000..These data suggest that myofibroblasts are the principal proliferating cell type that contributes to the progression of airway fibrosis after V(2)O(5) injury... 
Susceptibility of cyclooxygenase-2-deficient mice to pulmonary fibrogenesisJames 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...- IL-13 and IL-1beta promote lung fibroblast growth through coordinated up-regulation of PDGF-AA and PDGF-RalphaJennifer 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... - Susceptibility of signal transducer and activator of transcription-1-deficient mice to pulmonary fibrogenesisDianne M Walters
CIIT Centers for Health Research, P O Box 12137, Research Triangle Park, NC 27709, USA
Am J Pathol 167:1221-9. 2005.... - 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 fibroblastsJennifer 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... - Male sex hormones exacerbate lung function impairment after bleomycin-induced pulmonary fibrosisJames 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... - Vanadium-induced STAT-1 activation in lung myofibroblasts requires H2O2 and P38 MAP kinaseYi-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... - STAT-1 signaling in human lung fibroblasts is induced by vanadium pentoxide through an IFN-beta autocrine loopAurita 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... - Cyclooxygenase-2 deficiency exacerbates bleomycin-induced lung dysfunction but not fibrosisJeffrey 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... - Vanadium-induced HB-EGF expression in human lung fibroblasts is oxidant dependent and requires MAP kinasesJennifer 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)... - Regulation of PDGF and its receptors in fibrotic diseasesJames 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... - Respiratory syncytial virus infection reduces lung inflammation and fibrosis in mice exposed to vanadium pentoxideElizabeth 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... - Lung fibrotic responses to particle exposureJames 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.... 
Genomic analysis of human lung fibroblasts exposed to vanadium pentoxide to identify candidate genes for occupational bronchitisJennifer L Ingram
The Hamner Institutes for Health Sciences, Research Triangle Park, North Carolina 27709, USA
Respir Res 8:34. 2007....- 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 asthmaJennifer 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 - EGF and PDGF receptor tyrosine kinases as therapeutic targets for chronic lung diseasesJennifer 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... - p38 mitogen-activated protein kinase regulates growth factor-induced mitogenesis of rat pulmonary myofibroblastsAnnette 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...