Impact of Darunavir, Atazanavir and Lopinavir Boosted with Ritonavir on Cultured Human Endothelial Cells: Beneficial Effect of Pravastatin
Abstract
Background: HIV-infected patients administered long-term ritonavir-boosted protease inhibitors (PIs) are at a greater risk for developing cardiovascular diseases. Endothelial dysfunction is an initiating event in HIV-associated atherosclerosis. Cultured endothelial cells can be used as a model to compare the endothelial toxicity of different PIs. Methods: We compared the effect of darunavir (DRV), darunavir/ritonavir (DRV/r), lopinavir/ritonavir (LPV/r) and atazanavir/ritonavir (ATV/r), used at clinically relevant concentrations, on human coronary artery endothelial cell vascular function, oxidative stress, inflammation and senescence, and studied the effect of pravastatin on PI-induced alterations. Results: Vascular endothelial cell function, evaluated by the expression of endothelial nitric oxide synthase and the production of nitric oxide and endothelin-1, was unaffected by DRV or DRV/r, but altered by LPV/r or ATV/r. DRV or DRV/r did not alter, or mildly induced oxidative stress and inflammation (phosphorylation of p65/RelA-NFκB, secretion of IL-6 and IL-8), while ATV/r and LPV/r induced a marked increase. Secretion of sICAM or sVCAM, indicative of altered cell integrity, was not or weakly altered by DRV or DRV/r, but increased by 2–3-fold by LPV/r or ATV/r. Similar results were observed regarding senescence markers: SA-β-galactosidase activation and overexpression of phospho-p53, p16 ink4 , p21 WAF-1 and prelamin A. Pravastatin could, in part, reverse PI-induced adverse effects. Conclusions: Ritonavir-boosted PIs differentially induced vascular endothelial cell dysfunction, reactive oxygen species production, inflammation and senescence with no effect or a mild effect of DRV/r, an intermediate effect of ATV/r, and a stronger effect of LPV/r. Statins could, in part, protect the cells from PI-induced endothelial dysfunction.
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Senescent human arterial endothelial cells induced by protease inhibitors display reduced e-NOS expression and increased VCAM-1 secretion.
“Importantly, these senescent cells displayed reduced expression of endothelial nitric oxide synthase (e‐NOS), an enzyme responsible for NO synthesis, and increased secretion of VCAM‐1 (Lefèvre et al, 2010; Auclair et al, 2014; Afonso et al, 2017).”
From The struggle of a good friend getting old: cellular senescence in viral responses and therapy (2021) · cites this paper as Auclair et al, 2014
Protease inhibitors induce senescence in human arterial endothelial cells in vitro.
“Protease inhibitors are reported to induce senescence in human arterial endothelial cells in vitro.”
From The struggle of a good friend getting old: cellular senescence in viral responses and therapy (2021) · cites this paper as Auclair et al, 2014
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Self-citationHIV Exacerbates Atherosclerosis by Altering Macrophage Function
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- Authors
- Auclair, M., Afonso, P., Capel, E., Caron-Debarle, M., & Capeau, J.
- Affiliations
- Inserm (FR)
- INSERM, UMR_S 938, CDR Saint Antoine, F-75012, Paris, France
- Corresponding author
- Capeau, Jacqueline
- Venue
- Antiviral Therapy
- Publisher
- SAGE Publications
- Published
- 2013-11-01
- Volume
- 19
- Issue
- 8
- Pages
- 773-782
- ISSN
- 1359-6535 (ISSN-L)
- 2040-2058
- OpenAlex
- W2032586043
- Cited by
- 42
- References
- 57
- Citations by year
- 2026: 4 · 2025: 1 · 2024: 3 · 2023: 1 · 2022: 2 · 2021: 4 · 2020: 8 · 2019: 3 · 2018: 7 · 2017: 3 · 2016: 5 · 2015: 1
- FWCI
- 1.97
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Antiviral Therapy (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Emergency Medicine › HIV-related health complications and treatments
- Health Sciences › Medicine › Infectious Diseases › HIV/AIDS drug development and treatment
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Keywords
- HIV protease inhibitors, ritonavir-boosted protease inhibitors, darunavir, atazanavir, lopinavir, pravastatin, endothelial dysfunction, endothelial cell cytotoxicity, oxidative stress, inflammation, endothelial cell senescence, statins, HIV-associated cardiovascular disease, endothelial nitric oxide synthase, NF-κB, soluble intercellular adhesion molecule
- MeSH terms
- Atazanavir Sulfate, Darunavir, Cells, Cultured, Drug Synergism, Humans, Nitric Oxide, Oligopeptides, Pyridines, Sulfonamides, Cellular Senescence, Pravastatin, Oxidative Stress, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Anti-HIV Agents, Ritonavir, Endothelial Cells, Lopinavir
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