Crosstalk between glucocorticoids and mitogen-activated protein kinase signalling pathways

被引：98

作者：

Clark, AR ^{[1
]}

Lasa, M ^{[1
]}

机构：

[1] Univ London Imperial Coll Sci Technol & Med, Fac Med, Kennedy Inst Rheumatol Div, London W6 8LH, England

来源：

CURRENT OPINION IN PHARMACOLOGY | 2003年 / 3卷 / 04期

基金：

英国医学研究理事会;

关键词：

D O I：

10.1016/S1471-4892(03)00073-0

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Synthetic glucocorticoids are potent modulators of the immune system, and are clinically invaluable in the treatment of a wide variety of conditions. However, their use can be limited by harmful side effects, and their mechanisms of action remain poorly understood and controversial. It has recently been reported that glucocorticoids induce the expression of two genes that participate in cross-talk with the mitogen-activated protein kinase signalling pathways. It is possible that both therapeutic and harmful effects of glucocorticoids may be mediated by these genes.

引用

页码：404 / 411

页数：8

共 83 条

[1] Duration of calcineurin and Erk signals regulates CD4/CD8 lineage commitment of thymocytes [J].

Adachi, S ;

Iwata, M .

CELLULAR IMMUNOLOGY, 2002, 215 (01) :45-53

[2] Ligand-induced differentiation of glucocorticoid receptor (GR) trans-repression and transactivation:: preferential targetting of NF-κB and lack of I-κB involvement [J].

Adcock, IM ;

Nasuhara, Y ;

Stevens, DA ;

Barnes, PJ .

BRITISH JOURNAL OF PHARMACOLOGY, 1999, 127 (04) :1003-1011

[3] The anti-inflammatory action of glucocorticoids is mediated by cell type specific regulation of apoptosis [J].

Amsterdam, A ;

Sasson, R .

MOLECULAR AND CELLULAR ENDOCRINOLOGY, 2002, 189 (1-2) :1-9

[4] Glucocorticoid-induced leucine zipper inhibits the raf-extracellular signal-regulated kinase pathway by binding to Raf-1 [J].

Ayroldi, E ;

Zollo, O ;

Macchiarulo, A ;

Di Marco, B ;

Marchetti, C ;

Riccardi, C .

MOLECULAR AND CELLULAR BIOLOGY, 2002, 22 (22) :7929-7941

[5] Modulation of T-cell activation by the glucocorticoid-induced leucine zipper factor via inhibition of nuclear factor κB [J].

Ayroldi, E ;

Migliorati, G ;

Bruscoli, S ;

Marchetti, C ;

Zollo, O ;

Cannarile, L ;

D'Adamio, F ;

Riccardi, C .

BLOOD, 2001, 98 (03) :743-753

[6] Therapeutic benefit of a dissociated glucocorticoid and the relevance of in vitro separation of transrepression from transactivation activity [J].

Belvisi, MG ;

Wicks, SL ;

Battram, CH ;

Bottoms, SEW ;

Redford, JE ;

Woodman, P ;

Brown, TJ ;

Webber, SE ;

Foster, ML .

JOURNAL OF IMMUNOLOGY, 2001, 166 (03) :1975-1982

[7] Synthesis of glucocorticoid-induced leucine zipper (GILZ) by macrophages: an anti-inflammatory and immunosuppressive mechanism shared by glucocorticoids and IL-10 [J].

Berrebi, D ;

Bruscoli, S ;

Cohen, N ;

Foussat, A ;

Migliorati, G ;

Bouchet-Delbos, L ;

Maillot, MC ;

Portier, A ;

Couderc, J ;

Galanaud, P ;

Peuchmaur, M ;

Riccardi, C ;

Emilie, D .

BLOOD, 2003, 101 (02) :729-738

[8] NF-κB family of transcription factors:: Central regulators of innate and adaptive immune functions [J].

Caamaño, J ;

Hunter, CA .

CLINICAL MICROBIOLOGY REVIEWS, 2002, 15 (03) :414-+

[9] 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

[10] Cloning, chromosomal assignment and tissue distribution of human GILZ, a glucocorticoid hormone-induced gene [J].

Cannarile, L ;

Zollo, O ;

D'Adamio, F ;

Ayroldi, E ;

Marchetti, C ;

Tabilio, A ;

Bruscoli, S ;

Riccardi, C .

CELL DEATH AND DIFFERENTIATION, 2001, 8 (02) :201-203

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