CD40 ligation protects bronchial epithelium against oxidant-induced caspase-independent cell death (Articolo in rivista)

Type
Label
  • CD40 ligation protects bronchial epithelium against oxidant-induced caspase-independent cell death (Articolo in rivista) (literal)
Anno
  • 2006-01-01T00:00:00+01:00 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
  • 10.1165/rcmb.2005-0433OC (literal)
Alternative label
  • Merendino AM, 1; Bucchieri F, 2; Gagliardo R, 3; Daryadel A, 4; Pompeo F, 3; Chiappara G, 3; Santagata R, 1; Bellia V, 1; David S, 2; Farina F, 2; Davies DE, 5; Simon HU, 4; Vignola AM 1, 3. (2006)
    CD40 ligation protects bronchial epithelium against oxidant-induced caspase-independent cell death
    in American journal of respiratory cell and molecular biology
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Merendino AM, 1; Bucchieri F, 2; Gagliardo R, 3; Daryadel A, 4; Pompeo F, 3; Chiappara G, 3; Santagata R, 1; Bellia V, 1; David S, 2; Farina F, 2; Davies DE, 5; Simon HU, 4; Vignola AM 1, 3. (literal)
Pagina inizio
  • 155 (literal)
Pagina fine
  • 164 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 35 (literal)
Rivista
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo
  • 2 (literal)
Note
  • ISI Web of Science (WOS) (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • 1 Department of Medicine, Pneumology, Physiology, and Human Nutrition; 2 Department of Experimental Medicine, Section of Human Anatomy, Universita` di Palermo, Palermo; 3 Institute of Biomedicine and Molecular Immunology (IBIM), Italian National Research Council, Palermo, Italy; 4 Department of Pharmacology, University of Bern, Bern, Switzerland 5 Division of Infection, Inflammation, and Repair, University of Southampton, United Kingdom; (literal)
Titolo
  • CD40 ligation protects bronchial epithelium against oxidant-induced caspase-independent cell death (literal)
Abstract
  • CD40 and its ligand regulate pleiotropic biological responses, including cell proliferation, differentiation, and apoptosis. In many inflammatory lung diseases, tissue damage by environmental or endogenous oxidants plays a major role in disease pathogenesis. As the epithelial barrier is a major target for these oxidants, we postulated that CD40, the expression of which is increased in asthma, plays a role in the regulation of apoptosis of bronchial epithelial cells exposed to oxidants. Using 16HBE 14o? cells exposed to oxidant stress, we found that ligation of CD40 (induced by G28-5 monoclonal antibodies) enhanced cell survival and increased the number of cells in G2/M (interphase between DNA synthesis and mitosis) of the cell cycle. This was associated with NF-?B and activator protein-1 activation and increased expression of the inhibitor of apoptosis, c-IAP1. However, oxidant stress-induced apoptosiswas found to be caspase- and calpain-independent implicating CD40 ligation as a regulator of caspase-independent cell death. This was confirmed by the demonstration that CD40 ligation prevented mitochondrial release and nuclear translocation of apoptosis inducing factor. In conclusion, we demonstrate a novel role for CD40 as a regulator of epithelial cell survival against oxidant stress. Furthermore, we have identified, for the first time, an endogenous inhibitory pathway of caspase-independent cell death. (literal)
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