HIV-1 Matrix Protein p17 Promotes Lymphangiogenesis and Activates the Endothelin-1/Endothelin B Receptor Axis
Author(s) -
Francesca Caccuri,
Christine Rueckert,
Cinzia Giagulli,
Kai Schulze,
Daniele Basta,
Sonia Zicari,
Stefania Marsico,
Edoardo Cervi,
Simona Fiorentini,
Mark Slevin,
Carlos A. Guzmán,
Arnaldo Caruso
Publication year - 2014
Publication title -
arteriosclerosis thrombosis and vascular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.007
H-Index - 270
eISSN - 1524-4636
pISSN - 1079-5642
DOI - 10.1161/atvbaha.113.302478
Subject(s) - lymphangiogenesis , lymphatic system , lymphatic endothelium , cancer research , chemokine receptor , biology , lymphatic vessel , endothelin 3 , lymph node , microbiology and biotechnology , matrigel , lymph node stromal cell , protein kinase b , chemokine , receptor , signal transduction , endothelin receptor , immunology , medicine , angiogenesis , inflammation , endothelins , metastasis , cancer , biochemistry
AIDS-related lymphomas are high grade and aggressively metastatic with poor prognosis. Lymphangiogenesis is essential in supporting proliferation and survival of lymphoma, as well as tumor dissemination. Data suggest that aberrant lymphangiogenesis relies on action of HIV-1 proteins rather than on a direct effect of the virus itself. HIV-1 matrix protein p17 was found to accumulate and persist in lymph nodes of patients even under highly active antiretroviral therapy. Because p17 was recently found to exert a potent proangiogenic activity by interacting with chemokine (C-X-C motif) receptors 1 and 2, we tested the prolymphangiogenic activity of the viral protein.
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