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HIV Promotes Atherosclerosis via Circulating Extracellular Vesicle MicroRNAs.

Andrea Da Fonseca Ferreira1, Jianqin Wei1,2, Lukun Zhang1

  • 1Interdisciplinary Stem Cell Institute, University of Miami Miller School of Medicine, Miami, FL 33136, USA.

International Journal of Molecular Sciences
|April 28, 2023
PubMed
Summary

People living with HIV (PLHIV) face higher cerebrocardiovascular disease (CVD) risks due to modified microRNAs in plasma extracellular vesicles (EVs). These EVs impair vascular cell function, contributing to increased atherosclerosis in PLHIV.

Keywords:
ECFCsHIVagingatherosclerosisextracellular vesiclesmiRNA

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Area of Science:

  • Cardiovascular Research
  • Virology
  • Molecular Biology

Background:

  • Individuals living with HIV (PLHIV) exhibit a significantly higher risk of cerebrocardiovascular diseases (CVD) compared to HIV-negative (HIVneg) individuals.
  • The precise biological mechanisms driving this elevated CVD risk in PLHIV remain incompletely understood.
  • A potential link involves alterations in plasma extracellular vesicles (EVs) and their impact on vascular health.

Purpose of the Study:

  • To investigate the role of microRNA (miR)-carrying extracellular vesicles (EVs) in plasma from PLHIV in the development of CVD.
  • To identify specific miRs within EVs that may mediate vascular dysfunction and atherosclerosis.
  • To explore therapeutic strategies targeting these miR-EV interactions.

Main Methods:

  • Comparative analysis of plasma EVs from PLHIV (N=74) and HIVneg individuals (N=23).
  • Assessment of atherosclerosis and endothelial colony-forming cell (ECFC) counts in PLHIV versus HIVneg cohorts.
  • In vivo studies using apoE-/- mice treated with EVs from PLHIV (HIVposEVs) or controls (HIVnegEVs).
  • Small RNA sequencing of EVs to identify differentially expressed miRs, focusing on let-7b-5p.
  • In vitro and in vivo experiments using mesenchymal stromal cell-derived tailored EVs (TEVs) loaded with let-7b-5p or its antagomir (miRZip-let-7b).

Main Results:

  • PLHIV demonstrated increased atherosclerosis and reduced ECFCs compared to HIVneg individuals.
  • HIVposEVs, but not control EVs, exacerbated atherosclerosis in mice, correlating with arterial cell and bone marrow cell (lin- BMCs) dysfunction.
  • Small RNA-seq identified let-7b-5p as a significantly overrepresented miR in HIVposEVs.
  • Therapeutic EVs engineered to inhibit let-7b-5p (miRZip-let-7b) counteracted the detrimental effects of HIVposEVs, while EVs delivering let-7b-5p mimicked these effects.
  • Overexpression of a let-7b-5p target gene, Hmga2, in lin- BMCs conferred protection against HIVposEVs-induced cellular changes.

Conclusions:

  • HIV-associated plasma extracellular vesicles, particularly those enriched with let-7b-5p, contribute to vascular dysfunction and atherosclerosis.
  • These findings elucidate a novel mechanism linking HIV infection to increased CVD risk.
  • Targeting specific microRNAs within EVs presents a potential therapeutic avenue for mitigating CVD in PLHIV.