Genomic and non-genomic effects of different glucocorticoids on mouse thymocyte apoptosis

被引:31
作者
Bruscoli, S
Di Virgilio, R
Donato, V
Velardi, E
Baldoni, M
Marchetti, C
Migliorati, G
Riccardi, C
机构
[1] Univ Perugia, Pharmacol Sect, Dept Clin & Expt Med, I-06100 Perugia, Italy
[2] Univ Perugia, Pharmacol Sect, Sch Med, Dept Clin & Expt Med, I-06122 Perugia, Italy
关键词
glucocorticoid; glucocorticoid-induced leucine zipper (GILZ); apoptosis; thymocyte; genomic effect; non-genomic effect;
D O I
10.1016/j.ejphar.2005.10.053
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Glucocorticoids, widely used therapeutic agents for several pathologies, act upon diverse cells and tissues, including the lympho-haemopoietic system. Glucocorticoid-mediated apoptosis has been described as one of the mechanisms underlying their pharmacological and physiological effects. Glucocorticoids induce apoptosis in thymocytes through genomic and non-genomic signals. We tested thymocyte apoptosis rates as induced by a panel of glucocorticoids. Using four glucocorticoids that are widely adopted in clinical practice we compared their induction of thymocyte apoptosis and activation of non-genomic and genomic signals, including phosphatidylinositol-specific phospholipase C (PI-PLC), caspase-8, -9 and -3, and Glucocorticoid-Induced Leucine Zipper (GILZ). GILZ is a protein that is rapidly induced by glucocorticoids treatment and involved in apoptosis modulation. Results indicate different glucocorticoids have different apoptotic activity which is related to their ability to induce both genomic, evaluated as caspases activation and GILZ expression, and non-genomic effects, evaluated as PI-PLC phosphorylation. (c) 2005 Elsevier B.V. All rights reserved.
引用
收藏
页码:63 / 70
页数:8
相关论文
共 42 条
[11]   ANALYSIS OF GLUCOCORTICOID ACTIONS ON RAT THYMOCYTE DEOXYRIBONUCLEIC-ACID BY FLUORESCENCE-ACTIVATED FLOW-CYTOMETRY [J].
COMPTON, MM ;
HASKILL, JS ;
CIDLOWSKI, JA .
ENDOCRINOLOGY, 1988, 122 (05) :2158-2164
[12]   Glucocorticoids act within minutes to inhibit recruitment of signalling factors to activated EGF receptors through a receptor-dependent, transcription-independent mechanism [J].
Croxtall, JD ;
Choudhary, Q ;
Flower, RJ .
BRITISH JOURNAL OF PHARMACOLOGY, 2000, 130 (02) :289-298
[13]   Different glucocorticoids vary in their genomic and non-genomic mechanism of action in A549 cells [J].
Croxtall, JD ;
van Hal, PTW ;
Choudhury, Q ;
Gilroy, DW ;
Flower, RJ .
BRITISH JOURNAL OF PHARMACOLOGY, 2002, 135 (02) :511-519
[14]   CORTICOSTEROID-MEDIATED IMMUNOREGULATION IN MAN [J].
CUPPS, TR ;
FAUCI, AS .
IMMUNOLOGICAL REVIEWS, 1982, 65 :133-155
[15]   A new dexamethasone-induced gene of the leucine zipper family protects T lymphocytes from TCR/CD3-activated cell death [J].
D'Adamio, F ;
Zollo, O ;
Moraca, R ;
Ayroldi, E ;
Bruscoli, S ;
Bartoli, A ;
Cannarile, L ;
Migliorati, G ;
Riccardi, C .
IMMUNITY, 1997, 7 (06) :803-812
[16]   Decrease of Bcl-xL and augmentation of thymocyte apoptosis in GILZ overexpressing transgenic mice [J].
Delfino, DV ;
Agostini, M ;
Spinicelli, S ;
Vito, P ;
Riccardi, C .
BLOOD, 2004, 104 (13) :4134-4141
[17]   Specific inhibition of glucocorticoid-induced thymocyte apoptosis by substance P [J].
Dimri, R ;
Sharabi, Y ;
Shoham, J .
JOURNAL OF IMMUNOLOGY, 2000, 164 (05) :2479-2486
[18]   Apoptosis of airway epithelial cells induced by corticosteroids [J].
Dorscheid, DR ;
Wojcik, KR ;
Sun, S ;
Marroquin, B ;
White, SR .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 2001, 164 (10) :1939-1947
[19]  
EAMSHAW WC, 1999, ANNU REV BIOCHEM, V68, P383, DOI DOI 10.1146/ANNUREV.BI0CHEM.68.1383
[20]   Acute cardiovascular protective effects of corticosteroids are mediated by non-transcriptional activation of endothelial nitric oxide synthase [J].
Hafezi-Moghadam, A ;
Simoncini, T ;
Yang, ZQ ;
Limbourg, FP ;
Plumier, JC ;
Rebsamen, MC ;
Hsieh, CM ;
Chui, DS ;
Thomas, KL ;
Prorock, AJ ;
Laubach, VE ;
Moskowitz, MA ;
French, BA ;
Ley, K ;
Liao, JK .
NATURE MEDICINE, 2002, 8 (05) :473-479