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LMNA Messenger RNA Expression in Highly Active Antiretroviral Therapy-Treated HIV-Positive Patients

Miranda, Merce PhD*; Chacón, Matilde R PhD*; Vidal, Francesc MD, PhD; Megia, Ana MD, PhD*; Richart, Cristóbal MD, PhD†‡; Veloso, Sergi MD; Saumoy, Maria MD; Olona, Carles MD§; Vendrell, Joan MD, PhD*

JAIDS Journal of Acquired Immune Deficiency Syndromes: December 1st, 2007 - Volume 46 - Issue 4 - p 384-389
doi: 10.1097/QAI.0b013e31815aba1b
Basic Science

The LMNA gene encodes for lamins A and C as major products, which are involved in nuclear stability, chromatin structure, and gene expression. Several LMNA mutations cause an insulin-resistant lipodystrophy that shares features with HIV-related lipodystrophy. Some HIV-treatment agents alter lamin A/C maturation, organization, and stability in 3T3-L1. We aimed to test the hypothesis that human adipose tissue LMNA expression can be altered in highly active antiretroviral therapy (HAART)-treated HIV-positive patients with lipodystrophy. We have also analyzed both isoforms and explored if their expression is associated with insulin resistance or inflammation in these patients. A cross-sectional study that analyzed abdominal subcutaneous adipose tissue from 39 treated HIV-positive patients (25 of whom had lipodystrophy) and 21 uninfected control subjects was performed. We have observed lower levels of lamin A isoform but normal levels of lamin C isoform in all HIV-infected patients, irrespective of the presence or absence of lipodystrophy, which reinforces the idea that an altered lamin A/C ratio could reflect a pathogenic condition. We have also found a correlation between LMNA adipose expression and several cytokine and adipogenic gene markers in HIV-positive patients, regardless of the presence or absence of lipodystrophy. Hence, in the present study, the lower lamin A expression observed in HIV-positive patients is related to HIV itself or to treatments rather than to the presence of lipodystrophy.

From the *Endocrinology and Diabetes Unit, Research Department, University Hospital of Tarragona Joan XXIII, “Pere Virgili” Institute, Rovira i Virgili University, Tarragona, Spain; †Internal Medicine Service, University Hospital of Tarragona Joan XXIII, “Pere Virgili” Institute, Rovira i Virgili University, Tarragona, Spain; ‡Centro de Investigación Biomédica en Red (CIBER) Pathophysiology of Obesity (CB/06), Girona, Spain; and §Surgery Service, University Hospital of Tarragona Joan XXIII, Tarragona, Spain.

Received for publication June 1, 2007; accepted September 10, 2007.

Funded by Marató TV3 (02/1830 and 02/1910); Fondo de Investigación Sanitaria (FIS) 02-1282; FIS 05-1994, FIS 05-1591; Fundación para la investigación y prevención del SIDA en España (FIPSE) 36610-06; and the Ministerio de Sanidad y Consumo, Instituto de Salud Carlos III, Red de Sida (RIS), Red de diabetes y enfermedades metabólicas (REDIMET) (RD06/0015/0011). Dr. Matilde R. Chacón is supported by a fellowship from the FIS CP06/00119.

Correspondence to: Merce Miranda, PhD, Unitat de Recerca, Hospital Universitari Joan XXIII de Tarragona, c/o Dr. Mallafré Guasch, 4, 43007 Tarragona, Spain (e-mail: mmiranda.hj23.ics@gencat.net).

© 2007 Lippincott Williams & Wilkins, Inc.