MICHAEL A O'REILLY

Summary

Affiliation: University of Rochester
Country: USA

Publications

  1. pmc Transdifferentiation of alveolar epithelial type II to type I cells is controlled by opposing TGF-β and BMP signaling
    Lan Zhao
    Dept of Pediatrics, Box 850, The Univ of Rochester, School of Medicine and Dentistry, 601 Elmwood Ave, Rochester NY 14642
    Am J Physiol Lung Cell Mol Physiol 305:L409-18. 2013
  2. pmc Neonatal hyperoxia alters the host response to influenza A virus infection in adult mice through multiple pathways
    Bradley W Buczynski
    Dept of Pediatrics, Box 850, The Univ of Rochester, School of Medicine and Dentistry, 601 Elmwood Ave, Rochester, NY 14642
    Am J Physiol Lung Cell Mol Physiol 305:L282-90. 2013
  3. pmc Neonatal oxygen increases sensitivity to influenza A virus infection in adult mice by suppressing epithelial expression of Ear1
    MICHAEL A O'REILLY
    Department of Pediatrics, The University of Rochester, Rochester, New York 14642, USA
    Am J Pathol 181:441-51. 2012
  4. ncbi request reprint The Cdk and PCNA domains on p21Cip1 both function to inhibit G1/S progression during hyperoxia
    Christopher E Helt
    Department of Enviromental Medicine, School of Medicine and Dentistry, The University of Rochester, Rochester, NY 14642, USA
    Am J Physiol Lung Cell Mol Physiol 286:L506-13. 2004
  5. ncbi request reprint p53-independent induction of GADD45 and GADD153 in mouse lungs exposed to hyperoxia
    M A O'Reilly
    Division of Neonatology, Department of Pediatrics, and Department of Radiation Oncology, School of Medicine and Dentistry, University of Rochester, Rochester, New York 14642, USA
    Am J Physiol Lung Cell Mol Physiol 278:L552-9. 2000
  6. ncbi request reprint Redox activation of p21Cip1/WAF1/Sdi1: a multifunctional regulator of cell survival and death
    MICHAEL A O'REILLY
    Department of Pediatrics, School of Medicine and Dentistry, University of Rochester, Rochester, NY 14642, USA
    Antioxid Redox Signal 7:108-18. 2005
  7. ncbi request reprint Type II epithelial cells are critical target for hyperoxia-mediated impairment of postnatal lung development
    Min Yee
    Department of Pediatrics, Box 850, University of Rochester, School of Medicine and Dentistry, 601 Elmwood Ave, NY 14642, USA
    Am J Physiol Lung Cell Mol Physiol 291:L1101-11. 2006
  8. pmc Neonatal hyperoxia enhances the inflammatory response in adult mice infected with influenza A virus
    MICHAEL A O'REILLY
    Department of Pediatrics, Box 850, University of Rochester School of Medicine and Dentistry, 601 Elmwood Avenue, Rochester, NY 14642, USA
    Am J Respir Crit Care Med 177:1103-10. 2008
  9. ncbi request reprint p21(Cip1/WAF1/Sdi1) does not affect expression of base excision DNA repair enzymes during chronic oxidative stress
    MICHAEL A O'REILLY
    Department of Pediatrics, School of Medicine and Dentistry, University of Rochester, Rochester, NY 14642, USA
    Antioxid Redox Signal 7:719-25. 2005
  10. ncbi request reprint Induced p21Cip1 in premature baboons with CLD: implications for alveolar hypoplasia
    MICHAEL A O'REILLY
    Dept of Pediatrics, Box 850, Univ of Rochester, 601 Elm wood Ave, Rochester, NY 14642, USA
    Am J Physiol Lung Cell Mol Physiol 285:L964-71. 2003

Research Grants

  1. TRANSFORMING GROWTH FACTOR BETA IN OXIDANT LUNG INJURY
    MICHAEL O REILLY; Fiscal Year: 1999
  2. Neonatal Oxygen and Susceptibility to Respiratory Viral Infections
    MICHAEL A contact O apos REILLY; Fiscal Year: 2010
  3. Cell Survival and Death in Oxidant Lung Injury
    MICHAEL A O apos REILLY; Fiscal Year: 2010
  4. Effect of Neonatal Hyperoxia on Alveolar Development and Infection
    MICHAEL A O apos REILLY; Fiscal Year: 2010
  5. Neonatal Oxygen and Susceptibility to Respiratory Viral Infections
    MICHAEL O REILLY; Fiscal Year: 2009
  6. Effect of Neonatal Hyperoxia on Alveolar Development and Infection
    MICHAEL O REILLY; Fiscal Year: 2009
  7. Cell Survival and Death in Oxidant Lung Injury
    MICHAEL O REILLY; Fiscal Year: 2009
  8. Cell Survival and Death in Oxidant Lung Injury
    MICHAEL O REILLY; Fiscal Year: 2007
  9. DNA Repair and Replication in Oxidant Lung Injury
    MICHAEL O REILLY; Fiscal Year: 2005
  10. DNA Repair and Replication in Oxidant Lung Injury
    MICHAEL O REILLY; Fiscal Year: 2004

Collaborators

Detail Information

Publications49

  1. pmc Transdifferentiation of alveolar epithelial type II to type I cells is controlled by opposing TGF-β and BMP signaling
    Lan Zhao
    Dept of Pediatrics, Box 850, The Univ of Rochester, School of Medicine and Dentistry, 601 Elmwood Ave, Rochester NY 14642
    Am J Physiol Lung Cell Mol Physiol 305:L409-18. 2013
    ..Together, these results suggest that the rate of ATII cell transdifferentiation is controlled by the opposing actions of BMP and TGF-β signaling that switch during the process of transdifferentiation. ..
  2. pmc Neonatal hyperoxia alters the host response to influenza A virus infection in adult mice through multiple pathways
    Bradley W Buczynski
    Dept of Pediatrics, Box 850, The Univ of Rochester, School of Medicine and Dentistry, 601 Elmwood Ave, Rochester, NY 14642
    Am J Physiol Lung Cell Mol Physiol 305:L282-90. 2013
    ..Therefore, these data suggest that multiple therapeutic strategies may be needed to provide complete protection against diseases attributed to prematurity and early life exposure to oxygen. ..
  3. pmc Neonatal oxygen increases sensitivity to influenza A virus infection in adult mice by suppressing epithelial expression of Ear1
    MICHAEL A O'REILLY
    Department of Pediatrics, The University of Rochester, Rochester, New York 14642, USA
    Am J Pathol 181:441-51. 2012
    ..People born prematurely may have defects in epithelial innate immunity that increase their risk for respiratory viral infections...
  4. ncbi request reprint The Cdk and PCNA domains on p21Cip1 both function to inhibit G1/S progression during hyperoxia
    Christopher E Helt
    Department of Enviromental Medicine, School of Medicine and Dentistry, The University of Rochester, Rochester, NY 14642, USA
    Am J Physiol Lung Cell Mol Physiol 286:L506-13. 2004
    ..Because PCNA also participates in DNA repair, these results raise the possibility that p21 also affects repair of oxidized DNA...
  5. ncbi request reprint p53-independent induction of GADD45 and GADD153 in mouse lungs exposed to hyperoxia
    M A O'Reilly
    Division of Neonatology, Department of Pediatrics, and Department of Radiation Oncology, School of Medicine and Dentistry, University of Rochester, Rochester, New York 14642, USA
    Am J Physiol Lung Cell Mol Physiol 278:L552-9. 2000
    ..These studies are consistent with the hypothesis that hyperoxia-induced DNA fragmentation is associated with the expression of GADD genes that may participate in DNA repair and/or apoptosis...
  6. ncbi request reprint Redox activation of p21Cip1/WAF1/Sdi1: a multifunctional regulator of cell survival and death
    MICHAEL A O'REILLY
    Department of Pediatrics, School of Medicine and Dentistry, University of Rochester, Rochester, NY 14642, USA
    Antioxid Redox Signal 7:108-18. 2005
    ..The recent appreciation that p21 regulates cell survival and death implies that it is a master regulator of cell fate. This review discusses how p21 can affect the cellular response to oxidative stress...
  7. ncbi request reprint Type II epithelial cells are critical target for hyperoxia-mediated impairment of postnatal lung development
    Min Yee
    Department of Pediatrics, Box 850, University of Rochester, School of Medicine and Dentistry, 601 Elmwood Ave, NY 14642, USA
    Am J Physiol Lung Cell Mol Physiol 291:L1101-11. 2006
    ..These data suggest that perinatal hyperoxia adversely affects alveolar development by disrupting the proper timing of type II cell proliferation and differentiation into type I cells...
  8. pmc Neonatal hyperoxia enhances the inflammatory response in adult mice infected with influenza A virus
    MICHAEL A O'REILLY
    Department of Pediatrics, Box 850, University of Rochester School of Medicine and Dentistry, 601 Elmwood Avenue, Rochester, NY 14642, USA
    Am J Respir Crit Care Med 177:1103-10. 2008
    ..Because survivors of BPD also show increased risk for symptomatic respiratory infections, we investigated how neonatal hyperoxia affected the response of adult mice infected with influenza A virus infection...
  9. ncbi request reprint p21(Cip1/WAF1/Sdi1) does not affect expression of base excision DNA repair enzymes during chronic oxidative stress
    MICHAEL A O'REILLY
    Department of Pediatrics, School of Medicine and Dentistry, University of Rochester, Rochester, NY 14642, USA
    Antioxid Redox Signal 7:719-25. 2005
    ..This suggests that p21 may protect oxidized cells by affecting the activity of BER enzymes and/or through other mechanisms, such as apoptosis...
  10. ncbi request reprint Induced p21Cip1 in premature baboons with CLD: implications for alveolar hypoplasia
    MICHAEL A O'REILLY
    Dept of Pediatrics, Box 850, Univ of Rochester, 601 Elm wood Ave, Rochester, NY 14642, USA
    Am J Physiol Lung Cell Mol Physiol 285:L964-71. 2003
    ..These data suggest that p21 may play a role in disorganized proliferation and alveolar hypoplasia seen in newborn chronic lung disease...
  11. ncbi request reprint Activation of the G2 cell cycle checkpoint enhances survival of epithelial cells exposed to hyperoxia
    MICHAEL A O'REILLY
    Department of Pediatrics, Box 850, School of Medicine and Dentistry, The University of Rochester, 601 Elmwood Avenue, Rochester, NY 14642, USA
    Am J Physiol Lung Cell Mol Physiol 284:L368-75. 2003
    ..These data indicate that hyperoxia rapidly inhibits proliferation after one cell cycle and that the G2 checkpoint is critical for limiting DNA damage and cell death...
  12. ncbi request reprint Bcl-2 family gene expression during severe hyperoxia induced lung injury
    M A O'Reilly
    Department of Pediatrics, School of Medicine and Dentistry, Children s Hospital at Strong, University of Rochester, New York 14642, USA
    Lab Invest 80:1845-54. 2000
    ..These findings suggest that oxygen-induced lung injury does not depend on the relative expression of these Bcl-2 members...
  13. ncbi request reprint The cyclin-dependent kinase inhibitor p21 protects the lung from oxidative stress
    M A O'Reilly
    Departments of Pediatrics Neonatology, School of Medicine and Dentistry, The University of Rochester, Rochester, New York, USA
    Am J Respir Cell Mol Biol 24:703-10. 2001
    ..Our findings have implications for patients suffering from the toxic effects of supplemental oxygen therapies...
  14. ncbi request reprint DNA damage and cell cycle checkpoints in hyperoxic lung injury: braking to facilitate repair
    M A O'Reilly
    Department of Pediatrics Neonatology, School of Medicine and Dentistry, University of Rochester, Rochester, New York 14642, USA
    Am J Physiol Lung Cell Mol Physiol 281:L291-305. 2001
    ..This review examines the effect of hyperoxia on DNA integrity, pulmonary cell proliferation, and cell cycle checkpoints activated by DNA damage...
  15. ncbi request reprint Growth arrest in G1 protects against oxygen-induced DNA damage and cell death
    Raymond C Rancourt
    Department of Environmental Medicine, The University of Rochester, Rochester, New York 14642, USA
    J Cell Physiol 193:26-36. 2002
    ..Our findings suggest that the protective effects of G1 is mediated not simply by a reduction in intracellular ROS, but rather through an enhanced ability to limit or rapidly recognize and repair damaged DNA...
  16. ncbi request reprint Loss of Gadd45a does not modify the pulmonary response to oxidative stress
    Jason M Roper
    Departments of Environmental Medicine, School of Medicine and Dentistry, University of Rochester, Rochester, NY 14642, USA
    Am J Physiol Lung Cell Mol Physiol 288:L663-71. 2005
    ..We conclude that increased tolerance of airway and type II epithelial cells to hyperoxia is not attributed solely to expression of Gadd45a...
  17. ncbi request reprint In vivo exposure to hyperoxia induces DNA damage in a population of alveolar type II epithelial cells
    Jason M Roper
    Dept of Pediatrics, Box 850, School of Medicine and Dentistry, Univ of Rochester, 601 Elmwood Ave, Rochester, NY 14642, USA
    Am J Physiol Lung Cell Mol Physiol 286:L1045-54. 2004
    ..These data reveal that type II cells exposed to in vivo hyperoxia have oxidized and fragmented DNA. Because type II cells are essential for lung remodeling, our findings raise the possibility that they are proficient in DNA repair...
  18. ncbi request reprint Identification and isolation of mouse type II cells on the basis of intrinsic expression of enhanced green fluorescent protein
    Jason M Roper
    Dept of Pediatrics, Box 850, School of Medicine and Dentistry, University of Rochester, 601 Elmwood Ave, Rochester, NY 14642, USA
    Am J Physiol Lung Cell Mol Physiol 285:L691-700. 2003
    ..This method will be invaluable for detecting and isolating mouse type II cells under a variety of experimental conditions...
  19. pmc Normal remodeling of the oxygen-injured lung requires the cyclin-dependent kinase inhibitor p21(Cip1/WAF1/Sdi1)
    Rhonda J Staversky
    Department of Pediatrics, School of Medicine and Dentistry, University of Rochester, Rochester, New York 14642, USA
    Am J Pathol 161:1383-93. 2002
    ..This observation has important implications for therapeutic strategies designed to attenuate long-term chronic lung disease after oxidant injury...
  20. ncbi request reprint Murine mechanical ventilation stimulates alveolar epithelial cell proliferation
    Patricia Rose Chess
    Departments of Pediatrics and Biomedical Engineering, University of Rochester, Rochester, New York 14642, USA patricia
    Exp Lung Res 36:331-41. 2010
    ..Ventilation did not increase apoptosis in alveolar type II cells, as measured by TUNEL staining. Ventilation at low tidal volumes leads to a mild inflammatory response and alveolar epithelial cell proliferation...
  21. pmc p21Cip1 protection against hyperoxia requires Bcl-XL and is uncoupled from its ability to suppress growth
    Peter F Vitiello
    Department of Environmental Medicine, Box 850, The University of Rochester, 601 Elmwood Ave, Rochester, NY 14642, USA
    Am J Pathol 168:1838-47. 2006
    ..Taken together, these data show that p21-mediated cytoprotection against hyperoxia involves regulation of Bcl-XL and is uncoupled from its ability to inhibit proliferation...
  22. pmc Transgenic extracellular superoxide dismutase protects postnatal alveolar epithelial proliferation and development during hyperoxia
    Richard L Auten
    Neonatal Perinatal Research Institute, Department of Pediatrics, Duke University Medical Center, Durham, North Carolina 27710, USA
    Am J Physiol Lung Cell Mol Physiol 290:L32-40. 2006
    ..Reducing the 95% O2-induced impairment of epithelial proliferation at a critical window of lung development was associated with protection against DNA damage and preservation of apical T1alpha expression at P3...
  23. pmc Epithelial ablation of Bcl-XL increases sensitivity to oxygen without disrupting lung development
    Rhonda J Staversky
    Department of Pediatrics, University of Rochester, NY 14642, USA
    Am J Respir Cell Mol Biol 43:376-85. 2010
    ....
  24. ncbi request reprint Ataxia telangiectasia mutated (ATM) and ATM and Rad3-related protein exhibit selective target specificities in response to different forms of DNA damage
    Christopher E Helt
    Department of Environmental Medicine, School of Medicine and Dentistry, The University of Rochester, Rochester, New York 14642, USA
    J Biol Chem 280:1186-92. 2005
    ..These data reveal activated ATM and ATR exhibit selective substrate specificity in response to different genotoxic agents...
  25. pmc p21(Cip1) protects against oxidative stress by suppressing ER-dependent activation of mitochondrial death pathways
    Peter F Vitiello
    Department of Environmental Medicine, The University of Rochester, NY 14642, USA
    Free Radic Biol Med 46:33-41. 2009
    ..Taken together, these data show that p21 integrates the DNA damage response with ER stress signaling, which then regulates mitochondrial death pathways during chronic genotoxic stress...
  26. pmc Neonatal hyperoxia causes pulmonary vascular disease and shortens life span in aging mice
    Min Yee
    Department of Pediatrics, School of Medicine and Dentistry, The University of Rochester, Rochester, New York, USA
    Am J Pathol 178:2601-10. 2011
    ..People exposed to hyperoxia as neonates may be at increased risk for pulmonary hypertension...
  27. pmc Lung development and the host response to influenza A virus are altered by different doses of neonatal oxygen in mice
    Bradley W Buczynski
    Department of Environmental Medicine, School of Medicine and Dentistry, The University of Rochester, 601 Elmwood Ave, Rochester, NY 14642, USA
    Am J Physiol Lung Cell Mol Physiol 302:L1078-87. 2012
    ..Our findings suggest that measuring lung function alone may not be sufficient to identify individuals born prematurely who have increased risk for respiratory viral infection...
  28. ncbi request reprint p21(Cip1/Waf1/Sdi1) protects against hyperoxia by maintaining expression of Bcl-X(L)
    Rhonda J Staversky
    Department of Pediatrics, The University of Rochester, Rochester, NY 14642, USA
    Free Radic Biol Med 41:601-9. 2006
    ..These findings reveal that p21-mediated protection against hyperoxia does not involve attenuation of p53-dependent apoptosis, but rather functions to maintain Bcl-X(L) expression during periods of persistent oxidative stress...
  29. pmc PUMA inactivation protects against oxidative stress through p21/Bcl-XL inhibition of bax death
    Peter F Vitiello
    Department of Environmental Medicine, School of Medicine and Dentistry, The University of Rochester, Rochester NY 14642, USA
    Free Radic Biol Med 44:367-74. 2008
    ..Enhanced survival was associated with increased Bcl-X(L) to block Bax activated cell death during oxidative stress...
  30. ncbi request reprint Increased epithelial cell proliferation in very premature baboons with chronic lung disease
    William M Maniscalco
    Division of Neonatology, Strong Children s Research Center, Department of Pediatrics, University of Rochester, Rochester, New York 14642, USA
    Am J Physiol Lung Cell Mol Physiol 283:L991-L1001. 2002
    ..These data show that the development of chronic lung disease is associated with major alterations in normal patterns of lung-cell proliferation...
  31. pmc Neonatal oxygen adversely affects lung function in adult mice without altering surfactant composition or activity
    Min Yee
    Dept of Pediatrics, Univ of Rochester, Rochester, NY 14642, USA
    Am J Physiol Lung Cell Mol Physiol 297:L641-9. 2009
    ..Furthermore, the disruptive effects of oxygen on epithelial development and lung mechanics are not equivalently dose dependent...
  32. ncbi request reprint p53 modulates radiation sensitivity independent of p21 transcriptional activation
    Dawn J Mazzatti
    Department of Pathology and Laboratory Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York, USA
    Am J Clin Oncol 28:43-50. 2005
    ..Together, these data indicate that p53 modulates radiation sensitivity in the G1 phase of the cell cycle through mechanisms independent of p53-mediated transcriptional activation of p21 and cell cycle arrest...
  33. pmc Parenchymal cell TNF receptors contribute to inflammatory cell recruitment and respiratory failure in Pneumocystis carinii-induced pneumonia
    Gloria 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...
  34. ncbi request reprint Hyperoxic ventilated premature baboons have increased p53, oxidant DNA damage and decreased VEGF expression
    William M Maniscalco
    Division of Neonatology, Children s Research Center, Pulmonary Biology and Disease Program, University of Rochester School of Medicine, Rochester, NY 14642, USA
    Pediatr Res 58:549-56. 2005
    ..The findings suggest that oxidant DNA damage may be a mechanism of increased p53 in hyperoxic fetal lung...
  35. pmc DNA damage induces downregulation of histone gene expression through the G1 checkpoint pathway
    Chuan Su
    Department of Biomedical Genetics, University of Rochester Medical Center, Rochester, NY 14642, USA
    EMBO J 23:1133-43. 2004
    ..Our results thus suggest that inhibition of Cdk2 activity following DNA damage results in the downregulation of histone gene transcription through dissociation of NPAT from histone gene clusters...
  36. pmc Hyperoxia augments ER-stress-induced cell death independent of BiP loss
    Jennifer S Gewandter
    Department of Biochemistry and Biophysics, The University of Rochester, Rochester, NY 14642, USA
    Free Radic Biol Med 47:1742-52. 2009
    ....
  37. pmc The RNA surveillance protein SMG1 activates p53 in response to DNA double-strand breaks but not exogenously oxidized mRNA
    Jennifer S Gewandter
    Department of Biochemistry and Biophysics, The University of Rochester, Rochester, NY, USA
    Cell Cycle 10:2561-7. 2011
    ....
  38. pmc Activation of the aryl hydrocarbon receptor during different critical windows in pregnancy alters mammary epithelial cell proliferation and differentiation
    Betina J Lew
    Department of Environmental Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York 14642, USA
    Toxicol Sci 111:151-62. 2009
    ..These varying outcomes in mammary development due to exposure at different times in pregnancy suggest there are critical windows during which AhR activation impairs mammary epithelial cell proliferation and differentiation...
  39. pmc The role of hyperoxia in the pathogenesis of experimental BPD
    Bradley W Buczynski
    Department of Environmental Medicine, The University of Rochester, School of Medicine and Dentistry, Rochester, NY, USA
    Semin Perinatol 37:69-78. 2013
    ....
  40. pmc Bcl-X(L) is the primary mediator of p21 protection against hyperoxia-induced cell death
    Yu Chieh M Wu
    Department of Biomedical Genetics, School of Medicine and Dentistry, The University of Rochester, Rochester, New York 14642, USA
    Exp Lung Res 37:82-91. 2011
    ..Altogether, these data suggest that Bcl-X(L) is the primary mediator by which p21 protects against hyperoxia-induced Bak/Bax-dependent cell death...
  41. pmc Acute tumor necrosis factor-alpha-induced liver injury in the absence of tumor necrosis factor receptor-associated factor 1 gene expression
    Gloria 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...
  42. ncbi request reprint Reactive oxidant and p42/44 MAP kinase signaling is necessary for mechanical strain-induced proliferation in pulmonary epithelial cells
    Patricia R Chess
    Department of Pediatrics, University of Rochester, New York, USA
    J Appl Physiol (1985) 99:1226-32. 2005
    ....
  43. pmc Disruption of p21 attenuates lung inflammation induced by cigarette smoke, LPS, and fMLP in mice
    Hongwei Yao
    Lung Biology and Disease Program, Department of Environmental Medicine, University of Rochester Medical Center, 601 Elmwood Ave, Box 850, Rochester, NY 14642, USA
    Am J Respir Cell Mol Biol 39:7-18. 2008
    ..These data may have ramifications in CS-induced senescence in the pathogenesis of chronic obstructive pulmonary disease/emphysema...
  44. pmc Neonatal hyperoxia increases sensitivity of adult mice to bleomycin-induced lung fibrosis
    Min Yee
    Department of Pediatrics, School of Medicine and Dentistry, University of Rochester, Rochester, NY 14642, USA
    Am J Respir Cell Mol Biol 48:258-66. 2013
    ....
  45. pmc Selective ablation of lung epithelial IKK2 impairs pulmonary Th17 responses and delays the clearance of Pneumocystis
    Nelissa Pérez-Nazario
    Department of Microbiology and Immunology, School of Medicine and Dentistry, University of Rochester, Rochester, NY 14642
    J Immunol 191:4720-30. 2013
    ..LECs likely set the threshold for initiation of the pulmonary immune response and serve to prevent exacerbated lung inflammation by promoting the rapid control of respiratory fungal infection. ..
  46. ncbi request reprint Macroarray analysis reveals a strain-induced oxidant response in pulmonary epithelial cells
    Patricia R Chess
    Department of Pediatrics, University of Rochester, Rochester, New York, USA
    Exp Lung Res 30:739-53. 2004
    ..Strain-induced oxidative stress was verified with the oxidant-sensitive dye dichlorodihydrofluorescein diacetate...
  47. pmc Memory CD8+ T cells are sufficient to alleviate impaired host resistance to influenza A virus infection caused by neonatal oxygen supplementation
    Matthew Giannandrea
    Department of Environmental Medicine, The University of Rochester, School of Medicine and Dentistry, Rochester, NY, USA
    Clin Vaccine Immunol 19:1432-41. 2012
    ..Our findings suggest that vaccines that generate robust T cell memory may be efficacious at reducing the increased sensitivity to respiratory viral infections in people born prematurely...
  48. ncbi request reprint c-Src interacts with and phosphorylates RelA/p65 to promote thrombin-induced ICAM-1 expression in endothelial cells
    Kaiser M Bijli
    Department of Pediatrics, Lung Biology and Disease Program, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA
    Am J Physiol Lung Cell Mol Physiol 292:L396-404. 2007
    ..These data implicate an important role of c-Src in phosphorylating RelA/p65 to promote the transcriptional activity of NF-kappaB and thereby ICAM-1 expression in endothelial cells...
  49. ncbi request reprint Carbonic anhydrase XII mRNA encodes a hydratase that is differentially expressed along the rabbit nephron
    George J Schwartz
    Department of Pediatrics, University of Rochester School of Medicine, Rochester, New York 14642, USA
    Am J Physiol Renal Physiol 284:F399-410. 2003
    ..Western blotting of expressed CA XII with two anti-rabbit CA IV peptide antibodies showed no cross-reactivity. Our findings indicate that CA XII may contribute to the membrane CA activity of proximal tubules and collecting ducts...

Research Grants17

  1. TRANSFORMING GROWTH FACTOR BETA IN OXIDANT LUNG INJURY
    MICHAEL O REILLY; Fiscal Year: 1999
    ..These studies are significant because understanding how ROS injure and kill pulmonary epithelial cells is critically important for improving clinical therapies that rely on supplemental oxygen. ..
  2. Neonatal Oxygen and Susceptibility to Respiratory Viral Infections
    MICHAEL A contact O apos REILLY; Fiscal Year: 2010
    ..End of Abstract) ..
  3. Cell Survival and Death in Oxidant Lung Injury
    MICHAEL A O apos REILLY; Fiscal Year: 2010
    ....
  4. Effect of Neonatal Hyperoxia on Alveolar Development and Infection
    MICHAEL A O apos REILLY; Fiscal Year: 2010
    ....
  5. Neonatal Oxygen and Susceptibility to Respiratory Viral Infections
    MICHAEL O REILLY; Fiscal Year: 2009
    ..End of Abstract) ..
  6. Effect of Neonatal Hyperoxia on Alveolar Development and Infection
    MICHAEL O REILLY; Fiscal Year: 2009
    ....
  7. Cell Survival and Death in Oxidant Lung Injury
    MICHAEL O REILLY; Fiscal Year: 2009
    ....
  8. Cell Survival and Death in Oxidant Lung Injury
    MICHAEL O REILLY; Fiscal Year: 2007
    ....
  9. DNA Repair and Replication in Oxidant Lung Injury
    MICHAEL O REILLY; Fiscal Year: 2005
    ..abstract_text> ..
  10. DNA Repair and Replication in Oxidant Lung Injury
    MICHAEL O REILLY; Fiscal Year: 2004
    ..abstract_text> ..
  11. DNA Repair and Replication in Oxidant Lung Injury
    MICHAEL O REILLY; Fiscal Year: 2003
    ..abstract_text> ..
  12. DNA Repair and Replication in Oxidant Lung Injury
    MICHAEL O REILLY; Fiscal Year: 2002
    ..abstract_text> ..
  13. TRANSFORMING GROWTH FACTOR BETA IN OXIDANT LUNG INJURY
    MICHAEL O REILLY; Fiscal Year: 2002
    ..These studies are significant because understanding how ROS injure and kill pulmonary epithelial cells is critically important for improving clinical therapies that rely on supplemental oxygen. ..
  14. TRANSFORMING GROWTH FACTOR BETA IN OXIDANT LUNG INJURY
    MICHAEL O REILLY; Fiscal Year: 2001
    ..These studies are significant because understanding how ROS injure and kill pulmonary epithelial cells is critically important for improving clinical therapies that rely on supplemental oxygen. ..
  15. TRANSFORMING GROWTH FACTOR BETA IN OXIDANT LUNG INJURY
    MICHAEL O REILLY; Fiscal Year: 2000
    ..These studies are significant because understanding how ROS injure and kill pulmonary epithelial cells is critically important for improving clinical therapies that rely on supplemental oxygen. ..
  16. Effect of Neonatal Hyperoxia on Alveolar Development and Infection
    MICHAEL A O apos REILLY; Fiscal Year: 2011
    ....