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Titolo:
Inflammatory cytokines synergize with the HIV-1 Tat protein to promote angiogenesis and Kaposi's sarcoma via induction of basic fibroblast growth factor and the alpha(v)beta(3)
Autore:
Barillari, G; Sgadari, C; Palladino, C; Gendelman, R; Caputo, A; Morris, CB; Nair, BC; Markham, P; Nel, A; Sturzl, M; Ensoli, B;
Indirizzi:
Ist Super Sanita, Virol Lab, I-00161 Rome, Italy Ist Super Sanita Rome Italy I-00161 nita, Virol Lab, I-00161 Rome, Italy Univ Ferrara, Dept Expt & Diagnost Med, I-44100 Ferrara, Italy Univ Ferrara Ferrara Italy I-44100 Diagnost Med, I-44100 Ferrara, Italy Tulane Univ, Med Ctr, Tulane Canc Ctr, Dept Pathol & Lab Med, New Orleans,LA 70112 USA Tulane Univ New Orleans LA USA 70112 & Lab Med, New Orleans,LA 70112 USA Adv Biosci Labs, Kensington, MD 20895 USA Adv Biosci Labs Kensington MD USA 20895 ci Labs, Kensington, MD 20895 USA Univ Calif Los Angeles, Dept Med, Div Clin Immunol & Allergy, Los Angeles,CA 90024 USA Univ Calif Los Angeles Los Angeles CA USA 90024 Los Angeles,CA 90024 USA Gesell Strahlen & Umweltforsch MbH, Natl Res Ctr Environm & Hlth, Inst MolVirol, D-8042 Neuherberg, Germany Gesell Strahlen & Umweltforsch MbH Neuherberg Germany D-8042 rg, Germany
Titolo Testata:
JOURNAL OF IMMUNOLOGY
fascicolo: 4, volume: 163, anno: 1999,
pagine: 1929 - 1935
SICI:
0022-1767(19990815)163:4<1929:ICSWTH>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; ACQUIRED IMMUNODEFICIENCY SYNDROME; IMMUNE-DEFICIENCY SYNDROME; ENDOTHELIAL-CELLS; SPINDLE CELLS; FACTOR-ALPHA; T-CELLS; FLK-1/KDR RECEPTOR; GENE-EXPRESSION; VIRUS TYPE-1;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
51
Recensione:
Indirizzi per estratti:
Indirizzo: Ensoli, B Ist Super Sanita, Virol Lab, Viale Regina Elena 299, I-00161 Rome, Italy Ist Super Sanita Viale Regina Elena 299 Rome Italy I-00161 taly
Citazione:
G. Barillari et al., "Inflammatory cytokines synergize with the HIV-1 Tat protein to promote angiogenesis and Kaposi's sarcoma via induction of basic fibroblast growth factor and the alpha(v)beta(3)", J IMMUNOL, 163(4), 1999, pp. 1929-1935

Abstract

The Tat protein of HIV-1, a transactivator of viral gene expression, is released by acutely infected T tells and, in this form, exerts angiogenic activities. These have linked the protein to the pathogenesis of Kaposi's sarcoma (KS), a vascular tumor frequent and aggressive in HIV-1-infected individuals (AIDS-KS), In this study, we show that a combination of the same inflammatory cytokines increased in KS lesions, namely IL-1 beta, TNF-alpha, and IFN-gamma, synergizes with Tat to promote in nude mice the development ofangioproliferative KS-like lesions that are not observed with each factor alone. Inflammatory cytokines induce the tissue expression of both basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF), two angiogenic molecules highly produced in primary KS lesions. However, bFGF, but not VEGF, synergizes with Tat in vivo and induces endothelial cells to migrate, to adhere, and to grow in response to Tat in vitro. Tar angiogenic effects correlate with the expression of the alpha(v)beta(3) integrin that is induced by bFGF and binds the arginine-glycine-aspartic acid (RGD) region of Tat, In contrast, no correlation is observed with the expression of alpha(v)beta(5), which is promoted by VEGF and binds Tat basic region. Finally, KS lesion formation induced by bFGF and Tat in nude mice is blocked by antagonists of RGD-binding integrins. Because alpha(v)beta(3) is an RGD-binding integrin that is highly expressed in primary KS lesions, where it colocalizes with extracellular Tat on vessels and spindle cells, these results suggest that alpha(v)beta(3) competitors may represent a new strategyfor the treatment of AIDS-KS.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 09/07/20 alle ore 13:37:40