Acetylcholine leads to signal transducer and activator of transcription 1 (STAT-1) mediated oxidative/nitrosative stress in human bronchial epithelial cell line (Articolo in rivista)

Type
Label
  • Acetylcholine leads to signal transducer and activator of transcription 1 (STAT-1) mediated oxidative/nitrosative stress in human bronchial epithelial cell line (Articolo in rivista) (literal)
Anno
  • 2013-01-01T00:00:00+01:00 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
  • 10.1016/j.bbadis.2013.06.009 (literal)
Alternative label
  • Profita M, Albano GD, Montalbano AM, Di Sano C, Anzalone G, Gagliardo R, Riccobono L, Bonanno A, Siena L, Pieper MP, Gjomarkaj M. (2013)
    Acetylcholine leads to signal transducer and activator of transcription 1 (STAT-1) mediated oxidative/nitrosative stress in human bronchial epithelial cell line
    in Biochimica et biophysica acta. Molecular basis of disease
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Profita M, Albano GD, Montalbano AM, Di Sano C, Anzalone G, Gagliardo R, Riccobono L, Bonanno A, Siena L, Pieper MP, Gjomarkaj M. (literal)
Pagina inizio
  • 1949 (literal)
Pagina fine
  • 1958 (literal)
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  • 1832 (literal)
Rivista
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#pagineTotali
  • 10 (literal)
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  • 12 (literal)
Note
  • PubMe (literal)
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  • a Unit: \"Ex vivo/In Vitro Models to study the Immunopathology and the Pharmacology of airway diseases\", Institute of Biomedicine and Molecular Immunology (IBIM), Italian National Research Council (CNR), Palermo, Italy b Dipartimento Biomedico di Medicina, Interna e Specialistica (Di.Bi.M.I.S.), Sezione di Pneumologia, University of Palermo, Palermo, Italy c Boehringer Ingelheim Pharma GmbH & Co. KG, Biberach, Germany (literal)
Titolo
  • Acetylcholine leads to signal transducer and activator of transcription 1 (STAT-1) mediated oxidative/nitrosative stress in human bronchial epithelial cell line (literal)
Abstract
  • The induction of nitric oxide synthase (iNOS) expression via the signal transducer and activator of transcription 1 (STAT-1) is involved in the mechanism of oxidative/nitrosative stress. We investigated whether acetylcholine (ACh) generates oxidative/nitrosative stress in bronchial epithelial cells during airway inflammation of COPD and evaluated the effects of Tiotropium, a once-daily antimuscarinic drug, and Olodaterol, a long-acting ?2-agonist on these mechanisms. Human bronchial epithelial cells (16-HBE) were stimulated (4h, 37°C) with induced sputum supernatants (ISSs) from healthy controls (HC) (n=10), healthy smokers (HS) (n=10) or COPD patients (n=10), as well as with ACh (from 1?M to 100?M). The activation of STAT-1 pathway (STAT-1Ser727 and STAT-1Tyr701) and iNOS was evaluated in the cell lysates by Western blot analysis as well as nitrotyrosine levels by ELISA, while reactive oxygen species (ROS) were evaluated by flow cytometry. Finally, the effect of Tiotropium (Spiriva®) (100nM), alone or in combination with Olodaterol (1nM), was tested in this model. ISSs from COPD patients significantly increased the phosphorylation of STAT-1Ser727 and STAT-1Tyr701, iNOS and ROS/Nitrotyrosine when compared with ISSs from HC or HS subjects in 16-HBE cells. Furthermore, synthetic ACh increased all these parameters in stimulated 16HBE when compared with untreated cells. Tiotropium and Olodaterol reduced the oxidative/nitrosative stress generated by ACh and ISSs. We concluded that ACh mediated the oxidative/nitrosative stress involving the STAT-1 pathway activation in human bronchial epithelial cells during COPD. ?2-Long acting and antimuscarinic drugs, normally used in the treatment of COPD as bronchodilator, might be able to control these cellular events. (literal)
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