Research Topics
Species | Scott BoitanoSummaryAffiliation: University of Arizona Country: USA Publications
Research Grants
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Detail Information
Publications
Development of highly potent protease-activated receptor 2 agonists via synthetic lipid tetheringAndrea N Flynn
2Department of Physiology, Arizona Respiratory Center, Arizona Health Sciences Center, 1501 N Campbell Ave, Tucson, AZ 85724 5030, USA
FASEB J 27:1498-510. 2013..Flynn, A. N., Hoffman, J., Tillu, D. V., Sherwood, C. L., Zhang, Z., Patek, R., Asiedu, M. N. K., Vagner, J., Price, T. J., Boitano, S. Development of highly potent protease-activated receptor 2 agonists via synthetic lipid tethering...
Laminin-332 alters connexin profile, dye coupling and intercellular Ca2+ waves in ciliated tracheal epithelial cellsBrant 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....- Alternaria alternata serine proteases induce lung inflammation and airway epithelial cell activation via PAR2Scott 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... - 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 vivoAndrea 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... - Lanthanide labeling of a potent protease activated receptor-2 agonist for time-resolved fluorescence analysisJustin 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... - Pulmonary biomarkers based on alterations in protein expression after exposure to arsenicR 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... - Chronic arsenic exposure in nanomolar concentrations compromises wound response and intercellular signaling in airway epithelial cellsCara 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... - Arsenic alters ATP-dependent Ca²+ signaling in human airway epithelial cell wound responseCara 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... - Tracheobronchial markers of lung injury in smoke inhalation victimsMargaret 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... - Arsenic upregulates MMP-9 and inhibits wound repair in human airway epithelial cellsColin 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... - Tracheobronchial protease inhibitors, body surface area burns, and mortality in smoke inhalationMargaret 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... 
Extracellular matrix-driven alveolar epithelial cell differentiation in vitroColin O Olsen
Arizona Respiratory Center, University of Arizona Health Sciences Center, Tucson, AZ 85724-5051, USA
Exp Lung Res 31:461-82. 2005....
Research Grants
- SPATIOTEMPORAL NITRIC OXIDE SIGNALING, AIRWAY EPITHELIUMScott 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. ..
- MODELING AIRWAY RESPONSE TO BORDETELLA SP INFECTIONScott 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. ..