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Am J Physiol Lung Cell Mol Physiol 284: L1112-L1120, 2003. First published February 21, 2003; doi:10.1152/ajplung.00178.2002
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Vol. 284, Issue 6, L1112-L1120, June 2003

Mitogen-activated protein kinases mediate peroxynitrite-induced cell death in human bronchial epithelial cells

Elodie Nabeyrat, Gina E. Jones, Peter S. Fenwick, Peter J. Barnes, and Louise E. Donnelly

Thoracic Medicine, National Heart and Lung Institute, Faculty of Medicine, Imperial College of Science, Technology and Medicine, London SW3 6LY, United Kingdom

Peroxynitrite, formed by the reaction of nitric oxide (NO · ) with superoxide anions (O<UP><SUB>2</SUB><SUP>−</SUP></UP>·), may play a role in the pathophysiology of inflammation. The effects of 3-morpholinosydnonimine (SIN-1), a peroxynitrite generator, on the human bronchial epithelial cell line BEAS-2B, were examined. SIN-1 exposure resulted in cell death in a time- and dose-dependent manner. Depletion of intracellular glutathione increased the vulnerability of the cells. Pretreatment with Mn(III)tetrakis(N-methyl-4'-pyridyl)porphyrin (MnTMPyP) or hydroxocobalamin (HC), O<UP><SUB>2</SUB><SUP>−</SUP></UP>· and NO · scavengers, respectively, reduced significantly SIN-1-induced cell death (18.66 ± 3.57 vs. 77.01 ± 14.07 or 82.20 ± 9.64, % cell viability SIN-1 vs. MnTMPyP or HC). Moreover, the mitogen-activated protein kinases (MAPK) p44/42 (ERK), p38, and p54/46 (JNK) were also activated in a time- and concentration-dependent manner. PD-98059 and SB-239063, specific inhibitors of ERK and p38 MAPK pathways, failed to protect cells against 1 mM SIN-1. However, PD-98059 partially inhibited (60% cell survival) SIN-1 effects at <= 0.25 mM, and this was increased with the inclusion of SB-239063. Therefore, MAPKs may mediate signal transduction pathways induced by peroxynitrite in lung epithelial cells leading to cell death.

BEAS-2B cells; superoxide; nitric oxide; nitrosative stress; 3-morpholinosydnonimine


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