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Titolo:
Thymosin alpha(1) is a time and dose-dependent antagonist of dexamethasone-induced apoptosis of murine thymocytes in vitro
Autore:
Baumann, CA; Badamchian, M; Goldstein, AL;
Indirizzi:
George Washington Univ, Sch Med & Hlth Sci, Dept Biochem & Mol Biol, Washington, DC 20037 USA George Washington Univ Washington DC USA 20037 , Washington, DC 20037 USA
Titolo Testata:
INTERNATIONAL JOURNAL OF IMMUNOPHARMACOLOGY
fascicolo: 12, volume: 22, anno: 2000,
pagine: 1057 - 1066
SICI:
0192-0561(200012)22:12<1057:TAIATA>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROGRAMMED CELL-DEATH; ENDOGENOUS ENDONUCLEASE ACTIVATION; THYMIC EPITHELIAL-CELLS; POSITIVE SELECTION; NEGATIVE SELECTION; IL-2 PROTECTS; LYMPHOCYTES; PATHWAYS; KINETICS; THYMOSIN-ALPHA(1);
Keywords:
thymosin; thymosin alpha(1); thymocyte apoptosis; thymocyte maturation;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
50
Recensione:
Indirizzi per estratti:
Indirizzo: Goldstein, AL George Washington Univ, Sch Med & Hlth Sci, Dept Biochem & Mol Biol, 2300 Eye St NW, Washington, DC 20037 USA George Washington Univ 2300 Eye St NW Washington DC USA 20037
Citazione:
C.A. Baumann et al., "Thymosin alpha(1) is a time and dose-dependent antagonist of dexamethasone-induced apoptosis of murine thymocytes in vitro", INT J IMMUN, 22(12), 2000, pp. 1057-1066

Abstract

It is well established that glucocorticoid hormones induce apoptosis in immature developing thymocytes. Thymocyte apoptotsis can be modulated by growth factors, anti-oxidants and adhesion receptors. We have previously demonstrated that thymosin alpha (1) (T alpha (1)) antagonizes dexamethasone-induced apoptosis of CD4(+)CD8(+) thymocytes. In the present study, we further characterize the dose and time dependence of T alpha (1)'s antagonism of dexamethasone-induced thymocyte apoptosis. Ta, is effective at concentrationsranging from 2 to 100 mug/10(6) thymocytes. T alpha (1),s pre-treatment isnecessary to achieve its anti-apoptotic activity. Tee, provides temporary protection to thymocytes by slowing dexamethasone's apoptotic activity up to 12 h post dexamethasone treatment. Additionally, T alpha (1)'s activity is not sensitive to cycloheximide treatment, suggesting T alpha (1)'s activity is independent of protein synthesis. Finally, Tee, is unable to antagonize apoptosis induced by the reactive oxygen species, H2O2. suggesting T alpha (1)'s antagonism of dexamethasone occurs at the early stages of dexamethasone-induced apoptosis, prior to the production of reactive oxygen species. This evidence suggests that Ta, may provide a mechanism to transiently extend the life of a thymocyte during thymic selection. (C) 2000 International Society for Immunopharmacology. Published by Elsevier Science Ltd. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/09/20 alle ore 13:04:30