Premium
Role of FAP48 in HIV‐associated lipodystrophy
Author(s) -
Esposito Vincenzo,
Manente Lucrezia,
Lucariello Angela,
Perna Angelica,
Viglietti Rosaria,
Gargiulo Miriam,
Parrella Roberto,
Parrella Giovanni,
Baldi Alfonso,
De Luca Antonio,
Chirianni Antonio
Publication year - 2012
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.24221
Subject(s) - lipodystrophy , saquinavir , stavudine , lipoatrophy , efavirenz , indinavir , amprenavir , dyslipidemia , drug repositioning , medicine , metabolic syndrome , adipogenesis , calcineurin , integrase inhibitor , diabetes mellitus , pharmacology , antiretroviral therapy , immunology , human immunodeficiency virus (hiv) , endocrinology , biology , drug , adipose tissue , viral load , enzyme , protease , biochemistry , hiv 1 protease , transplantation
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. J. Cell. Biochem. 113: 3446–3454, 2012. © 2012 Wiley Periodicals, Inc.