Fibroblast Growth Factor-2 and the HIV-1 Tat Protein Synergize in Promoting Bcl-2 Expression and Preventing Endothelial Cell Apoptosis: Implications for the Pathogenesis of AIDS-Associated Kaposi's Sarcoma

Kaposi's sarcoma (KS) is a vascular tumor frequently occurring in Human Immunodeficiency Virus- (HIV-) 1-infected individuals. Our previous work indicated that the angiogenic fibroblast growth factor (FGF)-2 and the Tat protein of HIV-1, both expressed in KS lesions of HIV-infected patients, sy...

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Main Authors: Cecilia Sgadari, Giovanni Barillari, Clelia Palladino, Stefania Bellino, Brunella Taddeo, Elena Toschi, Barbara Ensoli
Format: Article
Language:English
Published: Wiley 2011-01-01
Series:International Journal of Vascular Medicine
Online Access:http://dx.doi.org/10.1155/2011/452729
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author Cecilia Sgadari
Giovanni Barillari
Clelia Palladino
Stefania Bellino
Brunella Taddeo
Elena Toschi
Barbara Ensoli
author_facet Cecilia Sgadari
Giovanni Barillari
Clelia Palladino
Stefania Bellino
Brunella Taddeo
Elena Toschi
Barbara Ensoli
author_sort Cecilia Sgadari
collection DOAJ
description Kaposi's sarcoma (KS) is a vascular tumor frequently occurring in Human Immunodeficiency Virus- (HIV-) 1-infected individuals. Our previous work indicated that the angiogenic fibroblast growth factor (FGF)-2 and the Tat protein of HIV-1, both expressed in KS lesions of HIV-infected patients, synergize at inducing angioproliferative, KS-like lesions in mice. Here we show that the development of angioproliferative lesions promoted in mice by combined Tat and FGF-2 associates with an increase in the levels of expression of the antiapoptotic Bcl-2 protein. Upregulation of Bcl-2 expression by combined FGF-2 and Tat occurs also in vitro, and this protects human primary endothelial cells from programmed cell death. As Bcl-2 is expressed in human KS lesions in a fashion paralleling the progression of the disease, these findings suggest a molecular mechanism by which Tat and FGF-2 cooperate in KS maintenance and progression in HIV-infected individuals.
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institution Kabale University
issn 2090-2824
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language English
publishDate 2011-01-01
publisher Wiley
record_format Article
series International Journal of Vascular Medicine
spelling doaj-art-8b33b0fbab634b5cb2e90db38b2ff3272025-02-03T05:52:47ZengWileyInternational Journal of Vascular Medicine2090-28242090-28322011-01-01201110.1155/2011/452729452729Fibroblast Growth Factor-2 and the HIV-1 Tat Protein Synergize in Promoting Bcl-2 Expression and Preventing Endothelial Cell Apoptosis: Implications for the Pathogenesis of AIDS-Associated Kaposi's SarcomaCecilia Sgadari0Giovanni Barillari1Clelia Palladino2Stefania Bellino3Brunella Taddeo4Elena Toschi5Barbara Ensoli6National AIDS Center, Istituto Superiore di Sanità, 00161 Rome, ItalyNational AIDS Center, Istituto Superiore di Sanità, 00161 Rome, ItalyNational AIDS Center, Istituto Superiore di Sanità, 00161 Rome, ItalyNational AIDS Center, Istituto Superiore di Sanità, 00161 Rome, ItalyNational AIDS Center, Istituto Superiore di Sanità, 00161 Rome, ItalyNational AIDS Center, Istituto Superiore di Sanità, 00161 Rome, ItalyNational AIDS Center, Istituto Superiore di Sanità, 00161 Rome, ItalyKaposi's sarcoma (KS) is a vascular tumor frequently occurring in Human Immunodeficiency Virus- (HIV-) 1-infected individuals. Our previous work indicated that the angiogenic fibroblast growth factor (FGF)-2 and the Tat protein of HIV-1, both expressed in KS lesions of HIV-infected patients, synergize at inducing angioproliferative, KS-like lesions in mice. Here we show that the development of angioproliferative lesions promoted in mice by combined Tat and FGF-2 associates with an increase in the levels of expression of the antiapoptotic Bcl-2 protein. Upregulation of Bcl-2 expression by combined FGF-2 and Tat occurs also in vitro, and this protects human primary endothelial cells from programmed cell death. As Bcl-2 is expressed in human KS lesions in a fashion paralleling the progression of the disease, these findings suggest a molecular mechanism by which Tat and FGF-2 cooperate in KS maintenance and progression in HIV-infected individuals.http://dx.doi.org/10.1155/2011/452729
spellingShingle Cecilia Sgadari
Giovanni Barillari
Clelia Palladino
Stefania Bellino
Brunella Taddeo
Elena Toschi
Barbara Ensoli
Fibroblast Growth Factor-2 and the HIV-1 Tat Protein Synergize in Promoting Bcl-2 Expression and Preventing Endothelial Cell Apoptosis: Implications for the Pathogenesis of AIDS-Associated Kaposi's Sarcoma
International Journal of Vascular Medicine
title Fibroblast Growth Factor-2 and the HIV-1 Tat Protein Synergize in Promoting Bcl-2 Expression and Preventing Endothelial Cell Apoptosis: Implications for the Pathogenesis of AIDS-Associated Kaposi's Sarcoma
title_full Fibroblast Growth Factor-2 and the HIV-1 Tat Protein Synergize in Promoting Bcl-2 Expression and Preventing Endothelial Cell Apoptosis: Implications for the Pathogenesis of AIDS-Associated Kaposi's Sarcoma
title_fullStr Fibroblast Growth Factor-2 and the HIV-1 Tat Protein Synergize in Promoting Bcl-2 Expression and Preventing Endothelial Cell Apoptosis: Implications for the Pathogenesis of AIDS-Associated Kaposi's Sarcoma
title_full_unstemmed Fibroblast Growth Factor-2 and the HIV-1 Tat Protein Synergize in Promoting Bcl-2 Expression and Preventing Endothelial Cell Apoptosis: Implications for the Pathogenesis of AIDS-Associated Kaposi's Sarcoma
title_short Fibroblast Growth Factor-2 and the HIV-1 Tat Protein Synergize in Promoting Bcl-2 Expression and Preventing Endothelial Cell Apoptosis: Implications for the Pathogenesis of AIDS-Associated Kaposi's Sarcoma
title_sort fibroblast growth factor 2 and the hiv 1 tat protein synergize in promoting bcl 2 expression and preventing endothelial cell apoptosis implications for the pathogenesis of aids associated kaposi s sarcoma
url http://dx.doi.org/10.1155/2011/452729
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