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Deciphering the molecular mechanisms involved in HIV-associated lipoatrophy by transcriptomics: a pilot study

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An Erratum to this article was published on 05 October 2017

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Abstract

HIV-associated lipoatrophy (LA) has considerable implications for risk of metabolic diseases, quality of life, and adherence to treatments. Although it has decreased in high-income countries, it is still very common in resource-limited countries. Understanding the pathophysiological mechanisms of LA can open the possibility to explore new ways to treat or prevent this condition. To identify new markers for an accurate and quick diagnosis will be also of interest. Thus, we aimed to examine functional classes of genes implicated in LA and to identify potential new markers for an accurate/quick diagnosis of LA and future complications. Eighteen participants were recruited: seven healthy volunteers, five non-LA-HIV patients, and six LA-HIV subjects. Clinical lipoatrophy was considered when changes in fat volume in the cheeks next to the nose, lateral aspect of the face, legs, arms, and buttocks were observed by the physicians. mRNA was isolated from peripheral blood mononuclear cells (PBMCs) to perform a transcriptomic and Gene Ontology analysis. To confirm RNA sequencing results, qPCRs were developed. A total of 55 genes were differentially expressed between LA and non-LA patients. Thirty-seven genes were overexpressed, whereas 18 genes were repressed. Functional analysis showed that overexpressed genes were involved in lymphocyte/neutrophil activation, inflammation, and atherogenesis. Several lymphoma markers and members of the lipocalin and aquaporin families were also found more expressed in LA patients. In contrast, most of the genes found less expressed in LA subjects were involved in angiogenesis and protection against myocardial infarction. Our results demonstrated a distinct transcriptomic signature in PBMCs of LA patients in comparison with non-LA-HIV subjects and, therefore, provided novel insights to the pathogenesis of HIV-associated lipoatrophy. Our study also highlights the potential usage of some of these genes as early markers of future complications.

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Change history

  • 05 October 2017

    Volume 73 issue 3 was published with an incorrect cover date. Correct is August 2017. The Publisher apologizes for this mistake and all related inconveniences caused by this.

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Acknowledgements

We appreciate the excellent technical assistance of Dr. Pérez-Martínez and the helpful pieces of advise from Dr. Larráyoz (CIBIR, Logroño, Spain). We thank the physicians from the Infectious Diseases Department (Hospital San Pedro, Logroño) for their help in the recruitment of subjects included in this study. We also thank all the subjects that collaborated in this study. This work was supported by Fundación Rioja Salud (FRS). FRS had no role in study design, data collection, and analysis, decision to publish, or preparation of the manuscript.

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Correspondence to Patricia Pérez-Matute.

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Patricia Pérez-Matute and María Iñiguez contributed equally.

An erratum to this article is available at https://doi.org/10.1007/s13105-017-0593-x.

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Pérez-Matute, P., Iñiguez, M., Recio-Fernández, E. et al. Deciphering the molecular mechanisms involved in HIV-associated lipoatrophy by transcriptomics: a pilot study. J Physiol Biochem 73, 431–443 (2016). https://doi.org/10.1007/s13105-016-0547-8

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