Mitogen-activated protein kinases and asthma

被引:87
作者
Pelaia, G
Cuda, G
Vatrella, A
Gallelli, L
Caraglia, M
Marra, M
Abbruzzese, A
Caputi, M
Maselli, R
Costanzo, FS
Marsico, SA
机构
[1] Magna Graecia Univ Catanzaro, Dept Expt & Clin Med, Chair Pharmacol, Catanzaro, Italy
[2] Univ Naples 2, Dept Cardiothorac & Resp Sci, Naples, Italy
[3] Univ Naples 2, Dept Biochem & Biophys, Naples, Italy
关键词
D O I
10.1002/jcp.20169
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Mitogen-activated protein kinases (MAPKs) are evolutionary conserved enzymes which play a key role in signal transduction mediated by cytokines, growth factors, neurotransmitters and various types of environmental stresses. In the airways, these extracellular stimuli elicit complex inflammatory and structural changes leading to the typical features of asthma including T cell activation, eosinophil and mast cell infiltration, as well as bronchial hyperresponsiveness and airway remodelling. Because MAPKs represent an important point of convergence for several different signalling pathways, they affect multiple aspects of normal airway function and also significantly contribute to asthma pathophysiology. Therefore, this review focuses on the crucial involvement of MAPKs in asthma pathogenesis, thus also discussing their emerging role as molecular targets for anti-asthma drugs. J. Cell. Physiol. (C) 2004 Wiley-Liss, Inc.
引用
收藏
页码:642 / 653
页数:12
相关论文
共 133 条
[11]   ERK1 and ERK2 activation by chemotactic factors in human eosinophils is interleukin 5-dependent and contributes to leukotriene C4 biosynthesis [J].
Bates, ME ;
Green, VL ;
Bertics, PJ .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (15) :10968-10975
[12]   SP600125, an anthrapyrazolone inhibitor of Jun N-terminal kinase [J].
Bennett, BL ;
Sasaki, DT ;
Murray, BW ;
O'Leary, EC ;
Sakata, ST ;
Xu, WM ;
Leisten, JC ;
Motiwala, A ;
Pierce, S ;
Satoh, Y ;
Bhagwat, SS ;
Manning, AM ;
Anderson, DW .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2001, 98 (24) :13681-13686
[13]  
Blease Kate, 2003, Expert Opin Emerg Drugs, V8, P71, DOI 10.1517/eoed.8.1.71.21043
[14]  
Boehme SA, 1999, J IMMUNOL, V163, P1611
[15]  
BORISH L, 1992, J IMMUNOL, V149, P3078
[16]   ERKS - A FAMILY OF PROTEIN-SERINE THREONINE KINASES THAT ARE ACTIVATED AND TYROSINE PHOSPHORYLATED IN RESPONSE TO INSULIN AND NGF [J].
BOULTON, TG ;
NYE, SH ;
ROBBINS, DJ ;
IP, NY ;
RADZIEJEWSKA, E ;
MORGENBESSER, SD ;
DEPINHO, RA ;
PANAYOTATOS, N ;
COBB, MH ;
YANCOPOULOS, GD .
CELL, 1991, 65 (04) :663-675
[17]   Asthmatic bronchial epithelium is more susceptible to oxidant-induced apoptosis [J].
Bucchieri, F ;
Puddicombe, SM ;
Lordan, JL ;
Richter, A ;
Buchanan, D ;
Wilson, SJ ;
Ward, J ;
Zummo, G ;
Howarth, PH ;
Djukanovic, R ;
Holgate, ST ;
Davies, DE .
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 2002, 27 (02) :179-185
[18]   Advances in immunology - Asthma [J].
Busse, WW ;
Lemanske, RF .
NEW ENGLAND JOURNAL OF MEDICINE, 2001, 344 (05) :350-362
[19]   Nuclear hormone receptor antagonism with AP-1 by inhibition of the JNK pathway [J].
Caelles, C ;
González-Sancho, JM ;
Muñoz, A .
GENES & DEVELOPMENT, 1997, 11 (24) :3351-3364
[20]  
Catena E, 1993, Monaldi Arch Chest Dis, V48, P6