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 Kaposis SarcomaReport as inadecuate




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 Kaposis Sarcoma - Download this document for free, or read online. Document in PDF available to download.

International Journal of Vascular MedicineVolume 2011 2011, Article ID 452729, 8 pages

Research Article

National AIDS Center, Istituto Superiore di Sanità, 00161 Rome, Italy

Department of Experimental Medicine, University of Rome Tor Vergata, 00133 Rome, Italy

Marjorie B. Kovler Viral Oncology Laboratories, The University of Chicago, Chicago, IL 60637, USA

Received 8 April 2011; Revised 18 July 2011; Accepted 24 July 2011

Academic Editor: Karlheinz Peter

Copyright © 2011 Cecilia Sgadari et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

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.





Author: Cecilia Sgadari, Giovanni Barillari, Clelia Palladino, Stefania Bellino, Brunella Taddeo, Elena Toschi, and Barbara Ensoli

Source: https://www.hindawi.com/



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