Role of FAP48 in HIV-associated lipodystrophy.

Vincenzo Esposito, Lucrezia Manente, Angela Lucariello, Angelica Perna, Rosaria Viglietti, Miriam Gargiulo, Roberto Parrella, Giovanni Parrella, Alfonso Baldi, Antonio De Luca, Antonio Chirianni

Index: J. Cell. Biochem. 113(11) , 3446-54, (2012)

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Abstract

The highly active antiretroviral therapy (HAART) can cause a metabolic syndrome consisting of lipodystropy/lipoatrophy, dyslipidemia, and type 2 diabetes mellitus with an increased cardiovascular risk. The pathogenetic bases of HAART-associated lipodystrophy are poorly known. A genetic screen was used to evaluate proteins that are modulated in HIV-1-infected patients with or without lipodystrophy syndrome, that are routinely treated with HAART regimens. The most significant modulation was represented by FAP48 expression. Stable over-expression of FAP48 was able to alter, in vitro, adipogenesis, acting both on calcineurin and glucocorticoid pathways. Finally, we demonstrated that FAP48 over-expression was able to influence the capacity of some HIV drugs, Saquinavir and Efavirenz, but not Stavudine, Amprenavir, and Indinavir to inhibit adipocyte formation. In conclusion, this molecule could be a potential target for novel therapeutic approaches to the HAART related lipodystrophy in HIV patients.Copyright © 2012 Wiley Periodicals, Inc.