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EnglishCD40 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.
Merendino, A., Bucchieri, F., Gagliardo, R., Daryadel, A., Pompeo, F., Chiappara, G., et al. (2006). CD40 Ligation Protects Bronchial Epithelium against Oxidant-Induced Caspase-Independent Cell Death. AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 35(2), 155-164 [10.1165/rcmb.2005-0433OC].
| Data di pubblicazione: | 2006 | |
| Titolo: | CD40 Ligation Protects Bronchial Epithelium against Oxidant-Induced Caspase-Independent Cell Death | |
| Autori: | ||
| Citazione: | Merendino, A., Bucchieri, F., Gagliardo, R., Daryadel, A., Pompeo, F., Chiappara, G., et al. (2006). CD40 Ligation Protects Bronchial Epithelium against Oxidant-Induced Caspase-Independent Cell Death. AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 35(2), 155-164 [10.1165/rcmb.2005-0433OC]. | |
| Rivista: | ||
| Digital Object Identifier (DOI): | http://dx.doi.org/10.1165/rcmb.2005-0433OC | |
| 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. | |
| Appare nelle tipologie: | 1.01 Articolo in rivista |
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