The Role of Mitogen-Activated Protein Kinases in Eotaxin-Induced Cytokine Production from Bronchial Epithelial Cells

2002 ◽  
Vol 27 (3) ◽  
pp. 329-335 ◽  
Author(s):  
Chang-Hao Cui ◽  
Tetsuya Adachi ◽  
Hajime Oyamada ◽  
Yumiko Kamada ◽  
Tomoe Kuwasaki ◽  
...  
2003 ◽  
Vol 284 (6) ◽  
pp. L1112-L1120 ◽  
Author(s):  
Elodie Nabeyrat ◽  
Gina E. Jones ◽  
Peter S. Fenwick ◽  
Peter J. Barnes ◽  
Louise E. Donnelly

Peroxynitrite, formed by the reaction of nitric oxide (NO · ) with superoxide anions (O[Formula: see text]·), 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[Formula: see text]· 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.


Pneumologie ◽  
2011 ◽  
Vol 65 (12) ◽  
Author(s):  
S Rim ◽  
S Jahan ◽  
G John ◽  
K Kohse ◽  
A Bohla ◽  
...  

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