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Blood, 1 March 2008, Vol. 111, No. 5, pp. 2806-2815. Prepublished online as a Blood First Edition Paper on December 3, 2007; DOI 10.1182/blood-2007-04-085555. This Article Full Text (PDF) All Versions of this Article: blood-2007-04-085555v1 111/5/2806    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Fonsato, V. Articles by Camussi, G. Search for Related Content PubMed PubMed Citation Articles by Fonsato, V. Articles by Camussi, G. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted April 17, 2007 Accepted November 26, 2007 PAX2 expression by HHV-8-infected endothelial cells induced a pro-angiogenic and pro-invasive phenotype Valentina Fonsato, Stefano Buttiglieri, Maria Chiara Deregibus, Benedetta Bussolati, Elisabetta Caselli, Dario Di Luca*, and Giovanni Camussi Department of Internal Medicine, Research Center for Experimental Medicine (CeRMS), and Center for Molecular Biotechnology, University of Torino, Torino, Italy Department Experimental and Diagnostic Medicine, Section of Microbiology, University of Ferrara, Ferrara, Italy * Corresponding author; email: ddl{at}unife.it. Human Herpesvirus 8 (HHV-8) is considered the primary etiologic agent of Kaposi's sarcoma (KS) and HHV-8 infected endothelial cells acquire a KS-like phenotype. In the present study we evaluated whether infection of microvascular endothelial cells (HMEC) with HHV-8 can trigger the expression of PAX2 oncogene and whether Pax2 protein is involved in HHV-8-induced transformation of HMEC. We found that HHV-8 infection induced the expression of both the PAX2 gene and Pax2 protein in HMEC but failed to induce Pax2 protein in HMEC stably transfected with PAX2 antisense (HMEC-AS). HHV-8-infected HMEC but not HMEC-AS acquired proinvasive proadhesive properties, enhanced survival and in vitro angiogenesis suggesting a correlation between Pax2 expression and the effects triggered by HHV-8 infection. When HMEC expressing Pax2 by stable transfection with PAX2 sense gene or by HHV-8 infection were implanted in vivo in SCID mice, enhanced angiogenesis and proliferative lesions resembling KS were observed. HHV-8 infected HMEC-AS failed to induce angiogenesis and KS-like lesions. These results suggest that the expression of Pax2 is required for the proangiogenic and proinvasive changes induced by HHV-8 infection in HMEC. In conclusion, HHV-8 infection may activate an embryonic angiogenic program in HMEC by inducing the expression of PAX2 oncogene. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: S. Bruno, C. Grange, M. C. Deregibus, R. A. Calogero, S. Saviozzi, F. Collino, L. Morando, A. Busca, M. Falda, B. Bussolati, et al. Mesenchymal Stem Cell-Derived Microvesicles Protect Against Acute Tubular Injury J. Am. Soc. Nephrol., May 1, 2009; 20(5): 1053 - 1067. [Abstract] [Full Text] [PDF]

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