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.