Circulating Microparticles Are Elevated in Treated HIV -1 Infection and Are Deleterious to Endothelial Cell Function
Author
Hijmans, Jamie GStockelman, Kelly A
Garcia, Vinicius
Levy, Ma'ayan V
Brewster, L Madden
Bammert, Tyler D
Greiner, Jared J
Stauffer, Brian L
Connick, Elizabeth
DeSouza, Christopher A
Affiliation
Univ Arizona, Div Infect DisIssue Date
2019-02-19
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WILEYCitation
Hijmans, J. G., Stockelman, K. A., Garcia, V., Levy, M. A. V., Brewster, L. M., Bammert, T. D., ... & DeSouza, C. A. (2019). Circulating Microparticles Are Elevated in Treated HIV‐1 Infection and Are Deleterious to Endothelial Cell Function. Journal of the American Heart Association, 8(4), e011134.Rights
Copyright © 2019 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell. This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs License.Collection Information
This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.Abstract
Background-Circulating microparticles have emerged as biomarkers and effectors of vascular disease. Elevated rates of cardiovascular disease are seen in HIV-1-seropositive individuals. The aims of this study were to determine: (1) if circulating microparticles are elevated in antiretroviral therapy-treated HIV-1-seropositive adults; and (2) the effects of microparticles isolated from antiretroviral therapy-treated HIV-1-seropositive adults on endothelial cell function, in vitro. Methods and Results-Circulating levels of endothelial-, platelet-, monocyte-, and leukocyte-derived microparticles were determined by flow cytometry in plasma from 15 healthy and 15 antiretroviral therapy-treated, virologically suppressed HIV-1-seropositive men. Human umbilical vein endothelial cells were treated with microparticles from individual subjects for 24 hours; thereafter, endothelial cell inflammation, oxidative stress, senescence, and apoptosis were assessed. Circulating concentrations of endothelial-, platelet-, monocyte-, and leukocyte-derived microparticles were significantly higher (approximate to 35%-225%) in the HIV-1-seropositive compared with healthy men. Microparticles from HIV-1-seropositive men induced significantly greater endothelial cell release of interleukin-6 and interleukin-8 (approximate to 20% and approximate to 35%, respectively) and nuclear factor-jB expression while suppressing anti-inflammatory microRNAs (miR-146a and miR-181b). Intracellular reactive oxygen species production and expression of reactive oxygen species-related heat shock protein 70 were both higher in cells treated with microparticles from the HIV-1-seropositive men. In addition, the percentage of senescent cells was significantly higher and sirtuin 1 expression lower in cells treated with HIV-1-related microparticles. Finally, caspase-3 was significantly elevated by microparticles from HIV-1-seropositive men. Conclusions-Circulating concentrations of endothelial-, platelet-, monocyte-, and leukocyte-derived microparticles were higher in antiretroviral therapy-treated HIV-1-seropositive men and adversely affect endothelial cells promoting cellular inflammation, oxidative stress, senescence, and apoptosis. Circulating microparticles may contribute to the vascular risk associated with HIV-1 infection.Note
Open Access JournalISSN
2047-9980PubMed ID
30779672Version
Final published versionSponsors
National Institutes of Health (NIH) [HL131458, HL135598]; NIH/National Center for Advancing Translational Sciences [UL1 TR001082]Additional Links
https://www.ahajournals.org/doi/full/10.1161/JAHA.118.011134ae974a485f413a2113503eed53cd6c53
10.1161/JAHA.118.011134
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Except where otherwise noted, this item's license is described as Copyright © 2019 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell. This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs License.
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