Research Topics
| Judith VoynowSummaryAffiliation: Duke University Medical Center Country: USA Publications
Research Grants
| Collaborators
|
Detail Information
Publications
NAD(P)H quinone oxidoreductase 1 regulates neutrophil elastase-induced mucous cell metaplasiaMarisa L Meyer
Department of Pediatrics, Duke University Medical Center, Durham, North Carolina 27710, USA
Am J Physiol Lung Cell Mol Physiol 303:L181-8. 2012..NQO1 is required for NE-induced inflammation and MCM. This model system demonstrates that NE-induced MCM directly correlates with inflammation, but not with oxidative stress...
Mucins, mucus, and sputumJudith A Voynow
Department of Pediatrics, Duke University School of Medicine, Durham, NC 27710, USA
Chest 135:505-12. 2009..This review will highlight the most recent insights on mucus biology in health and disease...
NAD(P)H quinone oxidoreductase 1 is essential for ozone-induced oxidative stress in mice and humansJudith A Voynow
Division of Pediatric Pulmonary Medicine, Department of Pediatrics, Duke University Medical Center, Box 2994, Durham, NC 27710, USA
Am J Respir Cell Mol Biol 41:107-13. 2009..Together, these results demonstrate that NQO1 modulates cellular redox status and influences the biologic and physiologic effects of ozone...
Proteases and cystic fibrosisJudith A Voynow
Department of Pediatrics, Duke University Medical Center, Box 2994, Durham, NC 27710, USA
Int J Biochem Cell Biol 40:1238-45. 2008..The mechanisms employed by proteases to impact airway function in CF will be reviewed...
Regulation of mucin genes in chronic inflammatory airway diseasesJudith A Voynow
Department of Pediatrics, Duke University Medical Center, Durham, NC 27710, USA
Am J Respir Cell Mol Biol 34:661-5. 2006....
Basal-like cells constitute the proliferating cell population in cystic fibrosis airwaysJudith A Voynow
Department of Pediatrics, Duke University Medical Center, Durham, NC, USA
Am J Respir Crit Care Med 172:1013-8. 2005..Cystic fibrosis airways are recurrently exposed to noxious stimuli, leading to epithelial injury. Previous reports suggest that cystic fibrosis airway epithelia may respond to injury by increasing proliferation...
Neutrophil elastase increases MUC5AC mRNA and protein expression in respiratory epithelial cellsJ A Voynow
Division of Pediatric Pulmonary Diseases, Duke University Medical Center, Durham, North Carolina 27710, USA
Am J Physiol 276:L835-43. 1999..Neutrophil elastase increased MUC5AC mRNA levels by enhancing mRNA stability. This is the first report of mucin gene regulation by this mechanism...
Neutrophil elastase induces mucus cell metaplasia in mouse lungJudith A Voynow
Department of Pediatrics, Duke University Medical Center, Box 2994, Durham, NC 27710, USA
Am J Physiol Lung Cell Mol Physiol 287:L1293-302. 2004..The addition of AAPV-CMK reduced these measures of inflammation to control levels. These experiments suggest that NE proteolytic activity initiates an inflammatory process leading to goblet cell metaplasia...
ErbB2 activity is required for airway epithelial repair following neutrophil elastase exposureBernard 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...
Neutrophil elastase inhibition of cell cycle progression in airway epithelial cells in vitro is mediated by p27kip1Bernard M Fischer
Division of Pediatric Pulmonary Medicine, Duke Univ Medical Center, Box 2994, Durham, NC 27710, USA
Am J Physiol Lung Cell Mol Physiol 293:L762-8. 2007..Our results demonstrate that p27 is regulated by NE and is critical for NE-induced cell cycle arrest...
Neutrophil elastase induces MUC5AC gene expression in airway epithelium via a pathway involving reactive oxygen speciesBernard M Fischer
Division of Pediatric Pulmonary Diseases, Duke University Medical Center, Durham, North Carolina 27710, USA
Am J Respir Cell Mol Biol 26:447-52. 2002..NE treatment increased cellular fluorescence in both cell types, indicating generation of intracellular reactive oxygen species. We conclude that NE treatment increases MUC5AC gene expression by an oxidant-dependent mechanism...
MARCKS-related peptide modulates in vivo the secretion of airway Muc5acW Michael Foster
Division of Pulmonary, and Critical Care Medicine, Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA
Am J Physiol Lung Cell Mol Physiol 299:L345-52. 2010....
Effects of TNFalpha on expression of ICAM-1 in human airway epithelial cells in vitro: oxidant-mediated pathways and transcription factorsThomas M Krunkosky
Department of Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, USA
Free Radic Biol Med 35:1158-67. 2003....
Regulation of MUC5AC expression by NAD(P)H:quinone oxidoreductase 1Shuo Zheng
Department of Pediatrics, Duke University Medical Center, Durham, NC 27710, USA
Free Radic Biol Med 42:1398-408. 2007..Our results indicate that NQO1 has an important role as a key mediator of NE-regulated oxidant stress and MUC5AC mucin gene expression...
Neutrophil elastase increases MUC4 expression in normal human bronchial epithelial cellsBernard M Fischer
Division of Pediatric Pulmonary Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA
Am J Physiol Lung Cell Mol Physiol 284:L671-9. 2003..Therefore, airway epithelial cells respond to neutrophil elastase exposure by increasing expression of MUC4, a potential activator of epithelial repair mechanisms...
What does mucin have to do with lung disease?Judith A Voynow
Division of Pediatric Pulmonary Diseases, Box 2994, Duke University Medical Center, Durham, NC 27710, USA
Paediatr Respir Rev 3:98-103. 2002..The insights gleaned from the investigations of mucin function and gene regulation should be useful for elucidating the cellular mechanisms leading to airway remodelling and mucus obstruction...
Neutrophil elastase increases airway epithelial nonheme iron levelsBernard M Fischer
Department of Pediatrics, Duke University Medical Center, Durham, NC, USA
Clin Transl Sci 2:333-9. 2009..We demonstrated in vitro that NE increased intracellular non-heme iron levels and degraded ferritin. Our results suggest that NE digests ferritin increasing the extracellular iron pool available for cellular uptake...
Respiratory tract mucin genes and mucin glycoproteins in health and diseaseMary Callaghan Rose
Research Center for Genetic Medicine, Room 5700, Children s National Medical Center, 111 Michigan Avenue NW, Washington, DC 20010, USA
Physiol Rev 86:245-78. 2006..The underlying premise is that understanding the pathways and processes that lead to mucus overproduction in specific airway diseases will allow circumvention or amelioration of these processes...
Research Grants
- NQO1: Linking Oxidant Stress to Inflammation in Airway Epithelial CellsJudith A Voynow; Fiscal Year: 2010..We hypothesize that NQO1 functions as a gate-keeper in airway epithelial cells to transmit ozone-generated oxidant stress to an inflammatory response which causes ozone-triggered airway disease. ..
- Mucin Gene Regulation by Elastase and OxidantsJudith Voynow; Fiscal Year: 2007..b. To determine whether NE and/or NQO1-generated ROS affect HuR binding to MUC5AC. c. To determine whether HuR binding is sufficient for MUC5AC mRNA stabilization. ..
- MUC4 Mucin and Airway Epithelial Regeneration in COPDJudith Voynow; Fiscal Year: 2006..Our ultimate goal is to use information from this project to identify new biologic targets for rational therapies to induce normal airway epithelial proliferation and differentiation following injury. ..
- REGULATION OF MUCIN GENE EXPRESSION BY ELASTASEJudith Voynow; Fiscal Year: 2003..The ultimate goal is to use information from this project to identify new biologic targets for therapeutic interventions to prevent mucus obstruction in chronic inflammatory airway diseases. ..
- NQO1: Linking Oxidant Stress to Inflammation in Airway Epithelial CellsJudith A Voynow; Fiscal Year: 2011..We hypothesize that NQO1 functions as a gate-keeper in airway epithelial cells to transmit ozone-generated oxidant stress to an inflammatory response which causes ozone-triggered airway disease. ..
