Scott Boitano

Summary

Affiliation: University of Arizona
Country: USA

Publications

  1. pmc Laminin-332 alters connexin profile, dye coupling and intercellular Ca2+ waves in ciliated tracheal epithelial cells
    Brant E Isakson
    Department of Molecular Physiology and Biological Physics, University of Virginia School of Medicine, University of Virginia Charlottesville, Virginia 22908, USA
    Respir Res 7:105. 2006
  2. pmc Alternaria alternata serine proteases induce lung inflammation and airway epithelial cell activation via PAR2
    Scott Boitano
    Dept of Physiology, Arizona Respiratory Center, Arizona Health Sciences Center, 1501 N Campbell Ave, Tucson, AZ, USA
    Am J Physiol Lung Cell Mol Physiol 300:L605-14. 2011
  3. pmc Development of highly potent protease-activated receptor 2 agonists via synthetic lipid tethering
    Andrea N Flynn
    Department of Physiology, Arizona Health Sciences Center, Tucson, AZ 85724 5030, USA
    FASEB J 27:1498-510. 2013
  4. ncbi request reprint Tracheobronchial protease inhibitors, body surface area burns, and mortality in smoke inhalation
    Margaret Kurzius-Spencer
    University of Arizona Mel and Enid Zuckerman College of Public Health, Community, Environment and Policy Division, Tucson, Arizona 85724, USA
    J Burn Care Res 30:824-31. 2009
  5. pmc Development and Evaluation of Small Peptidomimetic Ligands to Protease-Activated Receptor-2 (PAR2) through the Use of Lipid Tethering
    Scott Boitano
    Arizona Respiratory Center and Department of Physiology, University of Arizona, Tucson, Arizona, United States of America The BIO5 Collaborative Research Institute, University of Arizona, Tucson, Arizona, United States of America
    PLoS ONE 9:e99140. 2014
  6. pmc Chronic arsenic exposure in nanomolar concentrations compromises wound response and intercellular signaling in airway epithelial cells
    Cara L Sherwood
    Arizona Respiratory Center, University of Arizona, Tucson, AZ, USA
    Toxicol Sci 132:222-34. 2013
  7. pmc Arsenic upregulates MMP-9 and inhibits wound repair in human airway epithelial cells
    Colin E Olsen
    Arizona Respiratory Center, Arizona Health Sciences Center, 1501 N Campbell Ave, Tucson, AZ 85724 5030, USA
    Am J Physiol Lung Cell Mol Physiol 295:L293-302. 2008
  8. pmc Lanthanide labeling of a potent protease activated receptor-2 agonist for time-resolved fluorescence analysis
    Justin Hoffman
    Department of Physiology, Arizona Health Sciences Center, 1501 North Campbell Avenue, Tucson, AZ 85724 5030, USA
    Bioconjug Chem 23:2098-104. 2012
  9. pmc Potent agonists of the protease activated receptor 2 (PAR2)
    Scott Boitano
    Arizona Respiratory Center and Department of Physiology, University of Arizona, 1501 N Campbell Avenue, Tucson, Arizona 85724, United States
    J Med Chem 54:1308-13. 2011
  10. pmc The protease-activated receptor-2-specific agonists 2-aminothiazol-4-yl-LIGRL-NH2 and 6-aminonicotinyl-LIGRL-NH2 stimulate multiple signaling pathways to induce physiological responses in vitro and in vivo
    Andrea N Flynn
    Department of Physiology, BIO5 Collaborative Research Institute, Arizona Respiratory Center, Arizona Health Sciences Center, Tucson, Arizona 85724, USA
    J Biol Chem 286:19076-88. 2011

Collaborators

Detail Information

Publications18

  1. pmc Laminin-332 alters connexin profile, dye coupling and intercellular Ca2+ waves in ciliated tracheal epithelial cells
    Brant E Isakson
    Department of Molecular Physiology and Biological Physics, University of Virginia School of Medicine, University of Virginia Charlottesville, Virginia 22908, USA
    Respir Res 7:105. 2006
    ....
  2. pmc Alternaria alternata serine proteases induce lung inflammation and airway epithelial cell activation via PAR2
    Scott Boitano
    Dept of Physiology, Arizona Respiratory Center, Arizona Health Sciences Center, 1501 N Campbell Ave, Tucson, AZ, USA
    Am J Physiol Lung Cell Mol Physiol 300:L605-14. 2011
    ..alternata proteases act through PAR(2) to induce rapid increases in human airway epithelial [Ca(2+)](i) in vitro and cell recruitment in vivo. These responses are likely critical early steps in the development of allergic asthma...
  3. pmc Development of highly potent protease-activated receptor 2 agonists via synthetic lipid tethering
    Andrea N Flynn
    Department of Physiology, Arizona Health Sciences Center, Tucson, AZ 85724 5030, USA
    FASEB J 27:1498-510. 2013
    ..Our results demonstrate that the STL approach is a powerful tool for increasing ligand potency at PAR₂ and represent opportunities for drug development at other protease activated receptors and across GPCRs...
  4. ncbi request reprint Tracheobronchial protease inhibitors, body surface area burns, and mortality in smoke inhalation
    Margaret Kurzius-Spencer
    University of Arizona Mel and Enid Zuckerman College of Public Health, Community, Environment and Policy Division, Tucson, Arizona 85724, USA
    J Burn Care Res 30:824-31. 2009
    ..Initial SLPI levels predicted subsequent PAP. Increased early A2M in combination with extensive burn predicted early mortality...
  5. pmc Development and Evaluation of Small Peptidomimetic Ligands to Protease-Activated Receptor-2 (PAR2) through the Use of Lipid Tethering
    Scott Boitano
    Arizona Respiratory Center and Department of Physiology, University of Arizona, Tucson, Arizona, United States of America The BIO5 Collaborative Research Institute, University of Arizona, Tucson, Arizona, United States of America
    PLoS ONE 9:e99140. 2014
    ..Using the lipid-tethered-peptidomimetic approach we have developed novel structure activity relationships for PAR2 that allows for selective probing of PAR2 function across a broad range of physiological systems. ..
  6. pmc Chronic arsenic exposure in nanomolar concentrations compromises wound response and intercellular signaling in airway epithelial cells
    Cara L Sherwood
    Arizona Respiratory Center, University of Arizona, Tucson, AZ, USA
    Toxicol Sci 132:222-34. 2013
    ..Our findings demonstrate that chronic arsenic exposure at levels that are commonly found in drinking water (i.e., 10-50 ppb) alters cellular mechanisms critical to airway innate immunity...
  7. pmc Arsenic upregulates MMP-9 and inhibits wound repair in human airway epithelial cells
    Colin E Olsen
    Arizona Respiratory Center, Arizona Health Sciences Center, 1501 N Campbell Ave, Tucson, AZ 85724 5030, USA
    Am J Physiol Lung Cell Mol Physiol 295:L293-302. 2008
    ..We propose that arsenic in the airway can alter the airway epithelial barrier by restricting proper wound repair in part through the upregulation of MMP-9 by lung epithelial cells...
  8. pmc Lanthanide labeling of a potent protease activated receptor-2 agonist for time-resolved fluorescence analysis
    Justin Hoffman
    Department of Physiology, Arizona Health Sciences Center, 1501 North Campbell Avenue, Tucson, AZ 85724 5030, USA
    Bioconjug Chem 23:2098-104. 2012
    ..This ligand can serve as a critical tool in the screening and development of PAR(2) ligands...
  9. pmc Potent agonists of the protease activated receptor 2 (PAR2)
    Scott Boitano
    Arizona Respiratory Center and Department of Physiology, University of Arizona, 1501 N Campbell Avenue, Tucson, Arizona 85724, United States
    J Med Chem 54:1308-13. 2011
    ..Together these will lead to discovery of more potent agonists and antagonists of PAR(2)...
  10. pmc The protease-activated receptor-2-specific agonists 2-aminothiazol-4-yl-LIGRL-NH2 and 6-aminonicotinyl-LIGRL-NH2 stimulate multiple signaling pathways to induce physiological responses in vitro and in vivo
    Andrea N Flynn
    Department of Physiology, BIO5 Collaborative Research Institute, Arizona Respiratory Center, Arizona Health Sciences Center, Tucson, Arizona 85724, USA
    J Biol Chem 286:19076-88. 2011
    ..We have characterized three high potency ligands that can be used to explore the physiological role of PAR(2) in a variety of systems and pathologies...
  11. doi request reprint Tracheobronchial markers of lung injury in smoke inhalation victims
    Margaret Kurzius-Spencer
    Division of Community, Environment and Policy, University of Arizona Mel and Enid Zuckerman College of Public Health, Tucson, AZ 85724, USA
    J Burn Care Res 29:311-8. 2008
    ..013) and with a minimum Pao2/Fio2 >200 (P = .042) during 72 hours. In smoke inhalation victims, tracheobronchial IL-1beta and IL-8 increase rapidly and high initial IL-8 may predict improved oxygenation...
  12. pmc Arsenic compromises conducting airway epithelial barrier properties in primary mouse and immortalized human cell cultures
    Cara L Sherwood
    Arizona Respiratory Center, University of Arizona, Tucson, Arizona, United States of America Department of Cellular and Molecular Medicine, University of Arizona, Tucson, Arizona, United States of America Southwest Environmental Health Sciences Center, University of Arizona, Tucson, Arizona, United States of America Bio5 Collaborative Research Institute, University of Arizona, Tucson, Arizona, United States of America
    PLoS ONE 8:e82970. 2013
    ..These changes likely contribute to the observed arsenic-induced loss in basic innate immune defense and increased infection in the airway. ..
  13. pmc Arsenic alters ATP-dependent Ca²+ signaling in human airway epithelial cell wound response
    Cara L Sherwood
    Arizona Respiratory Center, Arizona Health Sciences Center, University of Arizona, Tucson, Arizona 85724 5030, USA
    Toxicol Sci 121:191-206. 2011
    ..g., ciliary beat, salt and water transport, bactericide production, and wound repair). Arsenic-induced compromise of such airway defense mechanisms may be an underlying contributor to chronic lung disease...
  14. pmc Environmental arsenic exposure, selenium and sputum alpha-1 antitrypsin
    Jefferey L Burgess
    Division of Community, Environment and Policy, Mel and Enid Zuckerman College of Public Health, University of Arizona, Tucson, Arizona, USA
    J Expo Sci Environ Epidemiol 24:150-5. 2014
    ..Reduction in AAT may be a means by which arsenic induces respiratory disease, and selenium may protect against this adverse effect. ..
  15. pmc Thrombospondin-1 and angiotensin II inhibit soluble guanylyl cyclase through an increase in intracellular calcium concentration
    Saumya Ramanathan
    Department of Molecular and Cellular Biology, University of Arizona, Tucson, Arizona 85721, United States
    Biochemistry 50:7787-99. 2011
    ..Taken together, these data suggest that sGC not only lowers [Ca(2+)](i) in response to NO, inducing vasodilation, but also is inhibited by high [Ca(2+)](i), providing a fine balance between signals for vasodilation and vasoconstriction...
  16. pmc Trichloroethylene disrupts cardiac gene expression and calcium homeostasis in rat myocytes
    Patricia T Caldwell
    Department of Veterinary Science and Microbiology, University of Arizona, Tucson, Arizona 85721, USA
    Toxicol Sci 104:135-43. 2008
    ..These results point to a novel area of TCE biology and, if confirmed in vivo, may help to explain the apparent cardio-specific toxicity of TCE exposure in the rodent embryo...
  17. pmc Pulmonary biomarkers based on alterations in protein expression after exposure to arsenic
    R Clark Lantz
    Department of Cell Biology and Anatomy, and Southwest Environmental Health Science Center, University of Arizona, 1501 N Campbell Avenue, Tucson, AZ 85724, USA
    Environ Health Perspect 115:586-91. 2007
    ..Our objective was to identify potential pulmonary protein biomarkers in the lung-lining fluid of mice chronically exposed to low-dose As and to validate these protein changes in human populations exposed to As...
  18. ncbi request reprint Extracellular matrix-driven alveolar epithelial cell differentiation in vitro
    Colin O Olsen
    Arizona Respiratory Center, University of Arizona Health Sciences Center, Tucson, AZ 85724 5051, USA
    Exp Lung Res 31:461-82. 2005
    ....

Research Grants5

  1. SPATIOTEMPORAL NITRIC OXIDE SIGNALING, AIRWAY EPITHELIUM
    Scott Boitano; Fiscal Year: 2002
    ..Additionally, new NO probes will be used to characterize unique spatiotemporal changes in cellular NO concentration that may elucidate its shift from a preventative to a damaging agent in the airway epithelium. ..
  2. MODELING AIRWAY RESPONSE TO BORDETELLA SP INFECTION
    Scott Boitano; Fiscal Year: 2001
    ..A greater understanding of bacterial/host interactions and their resulting physiological significance should lead to better development of prevention therapies and treatment strategies against bacterial invasion. ..
  3. SPATIOTEMPORAL NITRIC OXIDE SIGNALING, AIRWAY EPITHELIUM
    Scott Boitano; Fiscal Year: 2000
    ..Additionally, new NO probes will be used to characterize unique spatiotemporal changes in cellular NO concentration that may elucidate its shift from a preventative to a damaging agent in the airway epithelium. ..
  4. MODELING AIRWAY RESPONSE TO BORDETELLA SP INFECTION
    Scott Boitano; Fiscal Year: 2002
    ..A greater understanding of bacterial/host interactions and their resulting physiological significance should lead to better development of prevention therapies and treatment strategies against bacterial invasion. ..
  5. SPATIOTEMPORAL NITRIC OXIDE SIGNALING, AIRWAY EPITHELIUM
    Scott Boitano; Fiscal Year: 2001
    ..Additionally, new NO probes will be used to characterize unique spatiotemporal changes in cellular NO concentration that may elucidate its shift from a preventative to a damaging agent in the airway epithelium. ..