Luis A Ortiz

Summary

Affiliation: University of Pittsburgh
Country: USA

Publications

  1. pmc Systemic inhibition of NF-kappaB activation protects from silicosis
    Michelangelo Di Giuseppe
    Division of Occupational and Environmental Medicine, Department of Environmental and Occupational Health, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America
    PLoS ONE 4:e5689. 2009
  2. pmc Mesenchymal stem cell engraftment in lung is enhanced in response to bleomycin exposure and ameliorates its fibrotic effects
    Luis A Ortiz
    Division of Occupational Medicine, Department of Environmental and Occupational Health, University of Pittsburgh, Pittsburgh, PA 15261, USA
    Proc Natl Acad Sci U S A 100:8407-11. 2003
  3. pmc TNFR1/Phox Interaction and TNFR1 Mitochondrial Translocation Thwart Silica-Induced Pulmonary Fibrosis
    Fabrizio Fazzi
    Department of Environmental and Occupational Health, University of Pittsburgh, Pittsburgh, PA 15219
    J Immunol 192:3837-46. 2014
  4. doi request reprint Epithelial expression of TIMP-1 does not alter sensitivity to bleomycin-induced lung injury in C57BL/6 mice
    Cheryl L Fattman
    University of Pittsburgh, Graduate School of Public Health, Department of Environmental and Occupational Health, Bridgeside Point, 100 Technology Dr, Suite 328, Pittsburgh, PA 15219 3130, USA
    Am J Physiol Lung Cell Mol Physiol 294:L572-81. 2008
  5. ncbi request reprint Phosphorylation of tumor necrosis factor receptor 1 (p55) protects macrophages from silica-induced apoptosis
    Federica Gambelli
    Division of Occupational Medicine, Department of Environmental and Occupational Health, University of Pittsburgh, A731 Crabtree Hall, 130 De Soto Street, Pittsburgh, PA 15261, USA
    J Biol Chem 279:2020-9. 2004
  6. pmc Interleukin 1 receptor antagonist mediates the antiinflammatory and antifibrotic effect of mesenchymal stem cells during lung injury
    Luis A Ortiz
    Department of Environmental and Occupational Health, University of Pittsburgh, Pittsburgh, PA 15261, USA
    Proc Natl Acad Sci U S A 104:11002-7. 2007
  7. ncbi request reprint Molecular and functional properties of lung SP cells
    Susan D Reynolds
    Center for Lung Regeneration, Department of Environmental and Occupational Health, University of Pittsburgh, USA
    Am J Physiol Lung Cell Mol Physiol 292:L972-83. 2007
  8. pmc LPS-treated macrophage cytokines repress surfactant protein-B in lung epithelial cells
    Kiflai Bein
    Department of Environmental and Occupational Health, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA 15219 3130, USA
    Am J Respir Cell Mol Biol 49:306-15. 2013
  9. ncbi request reprint A multi-cyclone sampling array for the collection of size-segregated occupational aerosols
    Steven E Mischler
    a National Institute for Occupational Safety and Health, Office of Mine Safety and Health Research, Pittsburgh, Pennsylvania
    J Occup Environ Hyg 10:685-93. 2013
  10. pmc Pneumonic tularemia in rabbits resembles the human disease as illustrated by radiographic and hematological changes after infection
    Douglas S Reed
    Center for Vaccine Research, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America
    PLoS ONE 6:e24654. 2011

Collaborators

Detail Information

Publications17

  1. pmc Systemic inhibition of NF-kappaB activation protects from silicosis
    Michelangelo Di Giuseppe
    Division of Occupational and Environmental Medicine, Department of Environmental and Occupational Health, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America
    PLoS ONE 4:e5689. 2009
    ..Therefore, inhibition of NF-kappaB activation represents a potential therapeutic strategy for silicosis...
  2. pmc Mesenchymal stem cell engraftment in lung is enhanced in response to bleomycin exposure and ameliorates its fibrotic effects
    Luis A Ortiz
    Division of Occupational Medicine, Department of Environmental and Occupational Health, University of Pittsburgh, Pittsburgh, PA 15261, USA
    Proc Natl Acad Sci U S A 100:8407-11. 2003
    ..Collectively, these studies demonstrate that murine MSCs home to lung in response to injury, adopt an epithelium-like phenotype, and reduce inflammation and collagen deposition in lung tissue of mice challenged with BLM...
  3. pmc TNFR1/Phox Interaction and TNFR1 Mitochondrial Translocation Thwart Silica-Induced Pulmonary Fibrosis
    Fabrizio Fazzi
    Department of Environmental and Occupational Health, University of Pittsburgh, Pittsburgh, PA 15219
    J Immunol 192:3837-46. 2014
    ..7 macrophage survival to silica. These results identify TNFR1/Phox interaction as a key event in the pathogenesis of silicosis that prevents mtROS formation and reduces macrophage apoptosis. ..
  4. doi request reprint Epithelial expression of TIMP-1 does not alter sensitivity to bleomycin-induced lung injury in C57BL/6 mice
    Cheryl L Fattman
    University of Pittsburgh, Graduate School of Public Health, Department of Environmental and Occupational Health, Bridgeside Point, 100 Technology Dr, Suite 328, Pittsburgh, PA 15219 3130, USA
    Am J Physiol Lung Cell Mol Physiol 294:L572-81. 2008
    ..We conclude that although TIMP-1 expression is differentially regulated in fibrosis-sensitive and fibrosis-resistant strains, epithelial overexpression of TIMP-1 does not appear to substantially alter fibrotic lung disease in mice...
  5. ncbi request reprint Phosphorylation of tumor necrosis factor receptor 1 (p55) protects macrophages from silica-induced apoptosis
    Federica Gambelli
    Division of Occupational Medicine, Department of Environmental and Occupational Health, University of Pittsburgh, A731 Crabtree Hall, 130 De Soto Street, Pittsburgh, PA 15261, USA
    J Biol Chem 279:2020-9. 2004
    ..7 macrophages. These data suggest that NF-kappaB activation and ERK-mediated phosphorylation of the p55 TNF receptor are important cell survival mechanisms in the macrophage response to silica exposure...
  6. pmc Interleukin 1 receptor antagonist mediates the antiinflammatory and antifibrotic effect of mesenchymal stem cells during lung injury
    Luis A Ortiz
    Department of Environmental and Occupational Health, University of Pittsburgh, Pittsburgh, PA 15261, USA
    Proc Natl Acad Sci U S A 104:11002-7. 2007
    ..Identification of IL1RN-expressing human MSC subpopulations may provide a novel cellular vector for treating chronic inflammatory diseases in humans...
  7. ncbi request reprint Molecular and functional properties of lung SP cells
    Susan D Reynolds
    Center for Lung Regeneration, Department of Environmental and Occupational Health, University of Pittsburgh, USA
    Am J Physiol Lung Cell Mol Physiol 292:L972-83. 2007
    ..We conclude that the SP phenotype is common to clonogenic cells at multiple airway locations and suggest that Hoechst efflux is a property of cells expressing a wound-repair phenotype...
  8. pmc LPS-treated macrophage cytokines repress surfactant protein-B in lung epithelial cells
    Kiflai Bein
    Department of Environmental and Occupational Health, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA 15219 3130, USA
    Am J Respir Cell Mol Biol 49:306-15. 2013
    ....
  9. ncbi request reprint A multi-cyclone sampling array for the collection of size-segregated occupational aerosols
    Steven E Mischler
    a National Institute for Occupational Safety and Health, Office of Mine Safety and Health Research, Pittsburgh, Pennsylvania
    J Occup Environ Hyg 10:685-93. 2013
    ....
  10. pmc Pneumonic tularemia in rabbits resembles the human disease as illustrated by radiographic and hematological changes after infection
    Douglas S Reed
    Center for Vaccine Research, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America
    PLoS ONE 6:e24654. 2011
    ..Animal models of pneumonic tularemia with a pathophysiology similar to the human disease are needed to evaluate the efficacy of these potential medical countermeasures...
  11. ncbi request reprint Airway injury in lung disease pathophysiology: selective depletion of airway stem and progenitor cell pools potentiates lung inflammation and alveolar dysfunction
    Susan D Reynolds
    Department of Environmental and Occupational Health, University of Pittsburgh, Pittsburgh, PA 15260, USA
    Am J Physiol Lung Cell Mol Physiol 287:L1256-65. 2004
    ..On the basis of these data we conclude that selective airway injury can serve as the inciting injury in diseases characterized by severely compromised alveolar function...
  12. pmc Loss of fibroblast Thy-1 expression correlates with lung fibrogenesis
    James S Hagood
    Department of Pediatrics, University of Alabama, Birmingham, USA
    Am J Pathol 167:365-79. 2005
    ..These results suggest that fibrogenic injury promotes loss of lung fibroblast Thy-1 expression, resulting in enhanced fibrogenesis...
  13. ncbi request reprint Lung pathology in platelet-derived growth factor transgenic mice: effects of genetic background and fibrogenic agents
    Jian Li
    Section of Pulmonary Diseases, Critical Care and Environmental Medicine, Department of Medicine and Interdisciplinary Graduate Program in Molecular and Cellular Biology, Tulane University Health Sciences Center, New Orleans, Louisiana, USA
    Exp Lung Res 28:507-22. 2002
    ..These results demonstrate that the amount of PDGF-BB produced in wild-type mice is not a limiting factor in the development of bleomycin- or silica-induced pulmonary fibrosis...
  14. ncbi request reprint Bleomycin sensitivity of mice expressing dominant-negative p53 in the lung epithelium
    Sushmita Ghosh
    Program in Lung Biology, Section of Pulmonary Diseases, Critical Care and Environmental Medicine, Tulane Xavier Center for Bioenvironmental Research and Tualne Cancer Center, New Orleans, LA 70118, USA
    Am J Respir Crit Care Med 166:890-7. 2002
    ..These observations suggest that compromising p53 function in the alveolar epithelium impairs recovery of the lung from bleomycin-induced injury...
  15. ncbi request reprint Enalapril protects mice from pulmonary hypertension by inhibiting TNF-mediated activation of NF-kappaB and AP-1
    Luis A Ortiz
    Section of Pulmonary Diseases, Critical Care, and Environmental Medicine, Tulane University Medical Center, New Orleans, Louisiana 70112 2699, USA
    Am J Physiol Lung Cell Mol Physiol 282:L1209-21. 2002
    ..These results suggest that ACE inhibitor treatment decreases lung injury and the development of pulmonary hypertension in bleomycin-treated mice...
  16. pmc Stem cells and cell therapies in lung biology and lung diseases
    Daniel J Weiss
    Department of Medicine, University of Vermont College of Medicine, 149 Beaumont Avenue, HSRF 226, Burlington, VT 05405, USA
    Proc Am Thorac Soc 5:637-67. 2008
  17. ncbi request reprint Stem cells in lung biology
    Bruce R Pitt
    Am J Physiol Lung Cell Mol Physiol 286:L621-3. 2004

Research Grants13

  1. TNF-alpha Signaling in Silica-Induced Lung Fibrosis
    Luis Ortiz; Fiscal Year: 2002
    ..3). To determine whether overexpression of Tissue Inhibitor of Metalloproteinase 1 (TIMP-1) in mouse lung exacerbates silica- induced lung injury. ..
  2. TNF-alpha Signaling in Silica-Induced Lung Fibrosis
    Luis A Ortiz; Fiscal Year: 2010
    ..34 and 2.4 years for survival and graft rejection respectively). Consequently, these data indicate that silicosis still is a serious and frequently lethal lung disease for which no successful treatment is available. ..
  3. TNF-alpha Signaling in Silica-Induced Lung Fibrosis
    Luis Ortiz; Fiscal Year: 2009
    ..34 and 2.4 years for survival and graft rejection respectively). Consequently, these data indicate that silicosis still is a serious and frequently lethal lung disease for which no successful treatment is available. ..
  4. Mesenchymal Stem Cells in the Treatment of Lung Fibrosis
    Luis Ortiz; Fiscal Year: 2007
    ..3) To determine whether or not the systemic administration of MSCs can be used to ameliorate the fibroproliferative responses observed in the injured lung. ..
  5. TNF-alpha Signaling in Silica-Induced Lung Fibrosis
    Luis Ortiz; Fiscal Year: 2006
    ..3). To determine whether overexpression of Tissue Inhibitor of Metalloproteinase 1 (TIMP-1) in mouse lung exacerbates silica- induced lung injury. ..
  6. Mesenchymal Stem Cells in the Treatment of Lung Fibrosis
    Luis Ortiz; Fiscal Year: 2005
    ..3) To determine whether or not the systemic administration of MSCs can be used to ameliorate the fibroproliferative responses observed in the injured lung. ..
  7. TNF-alpha Signaling in Silica-Induced Lung Fibrosis
    Luis Ortiz; Fiscal Year: 2005
    ..3). To determine whether overexpression of Tissue Inhibitor of Metalloproteinase 1 (TIMP-1) in mouse lung exacerbates silica- induced lung injury. ..
  8. TNF-alpha Signaling in Silica-Induced Lung Fibrosis
    Luis Ortiz; Fiscal Year: 2004
    ..3). To determine whether overexpression of Tissue Inhibitor of Metalloproteinase 1 (TIMP-1) in mouse lung exacerbates silica- induced lung injury. ..
  9. TNF-alpha Signaling in Silica-Induced Lung Fibrosis
    Luis Ortiz; Fiscal Year: 2003
    ..3). To determine whether overexpression of Tissue Inhibitor of Metalloproteinase 1 (TIMP-1) in mouse lung exacerbates silica- induced lung injury. ..
  10. TNF-alpha Signaling in Silica-Induced Lung Fibrosis
    Luis Ortiz; Fiscal Year: 2002
    ..3). To determine whether overexpression of Tissue Inhibitor of Metalloproteinase 1 (TIMP-1) in mouse lung exacerbates silica- induced lung injury. ..
  11. TNF-alpha Signaling in Silica-Induced Lung Fibrosis
    Luis Ortiz; Fiscal Year: 2009
    ..34 and 2.4 years for survival and graft rejection respectively). Consequently, these data indicate that silicosis still is a serious and frequently lethal lung disease for which no successful treatment is available. ..