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Titolo:
HIV-1 Tat induces microvascular endothelial apoptosis through caspase activation
Autore:
Park, IW; Ullrich, CK; Schoenberger, E; Ganju, RK; Groopman, JE;
Indirizzi:
Harvard Univ, Inst Med, Beth Israel Deaconess Med Ctr, Div Expt Med,Sch Med, Boston, MA 02115 USA Harvard Univ Boston MA USA 02115 v Expt Med,Sch Med, Boston, MA 02115 USA
Titolo Testata:
JOURNAL OF IMMUNOLOGY
fascicolo: 5, volume: 167, anno: 2001,
pagine: 2766 - 2771
SICI:
0022-1767(20010901)167:5<2766:HTIMEA>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
KAPOSIS-SARCOMA; FLK-1/KDR RECEPTOR; DENDRITIC CELLS; GROWTH-FACTOR; CYTOCHROME-C; PROTEIN; ADHESION; EXPRESSION; BINDING; BCL-2;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
26
Recensione:
Indirizzi per estratti:
Indirizzo: Groopman, JE Harvard Univ, Inst Med, Beth Israel Deaconess Med Ctr, Div Expt Med,Sch Med, 4 Blackfan Circle,Room 309, Boston, MA 02115 USA Harvard Univ 4 Blackfan Circle,Room 309 Boston MA USA 02115 A
Citazione:
I.W. Park et al., "HIV-1 Tat induces microvascular endothelial apoptosis through caspase activation", J IMMUNOL, 167(5), 2001, pp. 2766-2771

Abstract

HIV-1 Tat, in addition to its critical role in viral transcription, is secreted from infected cells and can act as a proto-cytokine. We studied the effects of HIV-1 Tat in primary human microvascular endothelial cells of lung origin and found that it caused apoptosis. This apoptosis occurred without induction of either Fas or TNF, known mediators of programmed cell death. Tat, like Fas ligand, induced cleavage of chromatin structure, as evidenced by changes in DNA laddering, incorporation of fluorescein into the nickedchromosomal DNA (TUNEL assay), and mono- or oligonucleosomes. Furthermore,Tat treatment caused cleavage of poly(A/DP)-ribose polymerase, a substrateof caspases. Caspase-3, but not caspase-9, was activated following treatment of primary human microvascular endothelial cells of lung origin with either Tat or anti-Fas agonist Ab (anti-Fas). Inhibition of caspase-3 activitymarkedly reduced apoptosis. Although Fas-mediated apoptosis involved changes in Bcl-2, Bax, and Bad regulatory proteins, such alterations were not observed with Tat. Taken together, these data demonstrate that HIV-1 Tat is able to activate apoptosis in microvascular endothelium by a mechanism distinct from TNF secretion or the Fas pathway.

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Documento generato il 01/04/20 alle ore 11:25:22