Affiliation: University of Rochester
- Induction of chemokines by low-dose intratracheal silica is reduced in TNFR I (p55) null miceGloria S Pryhuber
Department of Pediatrics, Strong Children s Research Center, University of Rochester School of Medicine and Dentistry, Rochester, New York 14642, USA
Toxicol Sci 72:150-7. 2003..Silica dependent recruitment of neutrophils to the alveolar space and alveolar protein leak were, however, not altered by the absence of the TNF receptor...
- Parenchymal cell TNF receptors contribute to inflammatory cell recruitment and respiratory failure in Pneumocystis carinii-induced pneumoniaGloria S Pryhuber
Department of Pediatrics, University of Rochester Medical Center, Rochester, NY 14642, USA
J Immunol 181:1409-19. 2008..This study supports a key role of parenchymal cell TNFRs in lung injury induced by Pc and a potential protective effect of receptors on radiosensitive, bone marrow-derived cells...
- Acute tumor necrosis factor-alpha-induced liver injury in the absence of tumor necrosis factor receptor-associated factor 1 gene expressionGloria S Pryhuber
Department of Pediatrics, University of Rochester School of Medicine and Dentistry, Rochester, NY, USA
Am J Pathol 166:1637-45. 2005..These studies suggest that TRAF1 provides negative feedback for TNF-alpha synthesis and limits TNFRI-mediated systemic effects of TNF-alpha originating in the lung...
- The effects of interleukin-1beta in tumor necrosis factor-alpha-induced acute pulmonary inflammation in miceSara Saperstein
Department of Environmental Medicine, University of Rochester School of Medicine, Rochester, NY 14642, USA
Mediators Inflamm 2009:958658. 2009..These results suggest IL-1beta contributes, in part, to TNF-alpha-mediated, chemokine release, and neutrophil recruitment to the lung, potentially associated with altered soluble TNFR1 release into the BALF...
- G-protein-coupled receptor kinase interacting protein-1 is required for pulmonary vascular developmentJinjiang Pang
Aab Cardiovascular Research Institute and the Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA
Circulation 119:1524-32. 2009..However, there have been no in vivo studies of GIT1 function to date...
- Angiogenic factors and alveolar vasculature: development and alterations by injury in very premature baboonsWilliam M Maniscalco
Division of Neonatology, Strong Children s Research Center, Department of Pediatrics, University of Rochester, 601 Elmwood Ave, Rochester, NY 14642, USA
Am J Physiol Lung Cell Mol Physiol 282:L811-23. 2002..These data suggest that CLD impairs lung microvascular development and that a possible mechanism is disruption of VEGF and Flt-1 expression...
- Pathogenesis of bronchopulmonary dysplasiaPatricia R Chess
Department of Pediatrics, University of Rochester, Rochester, NY 14642, USA
Semin Perinatol 30:171-8. 2006..The contribution of hyperoxia and hypoxia, mechanical forces, vascular maldevelopment, inflammation, fluid management, patent ductus arteriosus (PDA), nutrition, and genetics will be discussed...
- TNF receptor signaling contributes to chemokine secretion, inflammation, and respiratory deficits during Pneumocystis pneumoniaTerry W Wright
Department of Pediatrics, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA
J Immunol 172:2511-21. 2004....
- IL-1beta augments TNF-alpha-mediated inflammatory responses from lung epithelial cellsSara Saperstein
Department of Environmental Medicine, University of Rochester School of Medicine, Rochester, New York 14642, USA
J Interferon Cytokine Res 29:273-84. 2009..These data suggest IL-1beta modulates TNF-alpha-mediated inflammatory lung diseases by enhancing epithelial cell TNF receptor surface expression...
- Hyperoxia and interferon-γ-induced injury in developing lungs occur via cyclooxygenase-2 and the endoplasmic reticulum stress-dependent pathwayRayman Choo-Wing
Division of Perinatal Medicine, Department of Pediatrics, Yale University School of Medicine, New Haven, CT 06520, USA
Am J Respir Cell Mol Biol 48:749-57. 2013..Cox2, via CHOP, may significantly contribute to the final common pathway of hyperoxia-induced and IFN-γ-mediated injury in developing lungs and human BPD...
- Effect of cumulative oxygen exposure on respiratory symptoms during infancy among VLBW infants without bronchopulmonary dysplasiaTimothy P Stevens
Division of Neonatology, Department of Pediatrics, University of Rochester, Rochester, New York, USA
Pediatr Pulmonol 45:371-9. 2010..A possible explanation for these inconsistent findings is that the cumulative dosage of neonatal supplemental oxygen to which infants are exposure is difficult to accurately quantify...
- Developmental regulation of p66Shc is altered by bronchopulmonary dysplasia in baboons and humansMatt K Lee
Center for Craniofacial Molecular Biology, School of Dentistry, University of Southren California, 2250 Alcazar Street, CSA 113, Los Angeles, CA 90033, USA
Am J Respir Crit Care Med 171:1384-94. 2005..The p66(Shc) adapter protein antagonizes mitogen-activated protein, or MAP, kinase, mediates oxidative stress, and is developmentally regulated in fetal mouse lungs...
- Secretoglobins SCGB3A1 and SCGB3A2 define secretory cell subsets in mouse and human airwaysSusan D Reynolds
Departments of Environmental and Occupational Health, and Pediatrics, University of Pittsburgh, Pennsylvania 15260, USA
Am J Respir Crit Care Med 166:1498-509. 2002..Altered expression of secretoglobins in airway disease may contribute to immunoregulatory perturbations commonly seen in chronic airway disease...
- TNFR ASSOCIATED FACTOR IN PULMONARY RESPONSE TO TNF-AGloria Pryhuber; Fiscal Year: 2003..The proposed studies will demonstrate the cellular function of TRAF1 in vitro and the role of TRAF1 expression in vivo in transgenic overexpression and ablation models stressed by hyperoxia. ..
- Cell Specific Responses to TNF-alpha in Lung FibrosisGloria Pryhuber; Fiscal Year: 2009..Lung disease caused by inhaled dust is a significant world wide health problem. This proposal will identify new targets for therapy of these chronic and often deadly diseases with reduced side effects. ..