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Influence of aspirin on SR-BI expression in human carotid plaques
Andreas Wehinger1, Ivan Tancevski, Ruediger Seiler
1Department of Internal Medicine, Innsbruck Medical University, Anichstrasse 35, Innsbruck, Austria.
Background:
We recently showed that aspirin promotes scavenger receptor class-B type I (SR-BI) protein expression in vitro in primary human macrophages and in vivo in resident peritoneal macrophages of mice.
Methods:
We compared SR-BI and CD68 expression in carotid atherosclerotic specimens from endarterectomized patients with (n=38) or without (n=19) low-dose aspirin medication (100 mg/day) prior to endarterectomy.
Results:
We found no differences concerning expression of CD68, indicating that aspirin did not influence macrophage content within atherosclerotic plaques. However, aspirin increased the expression of SR-BI protein in the analyzed specimens. In human THP-1-derived macrophages, induction of SR-BI protein by aspirin was abrogated by concomitant pharmacological inhibition of nuclear factor-kappa B (NF-kappaB). In in vitro experiments employing cultured primary macrophages from NF-kappaB/p50 KO mice, aspirin was not able to influence SR-BI expression. Additionally, no considerable effects on SR-BI expression were observed in vivo in resident macrophages of NF-kappaB/p50 KO mice orally treated with low or high doses of aspirin, respectively.
Conclusions:
We suggest that aspirin treatment might lead to enhanced expression of SR-BI in human plaque macrophages and that this effect is dependent on the presence of NF-kappaB.
Insights
Aspirin increases scavenger receptor class-B type I (SR-BI) protein in human atherosclerotic plaques. This effect is dependent on nuclear factor-kappa B (NF-kappaB) and does not alter macrophage content.
Area of Science:
- Cardiovascular Research
- Immunology
- Pharmacology
Background:
- Aspirin was previously shown to promote scavenger receptor class-B type I (SR-BI) protein expression in macrophages.
- SR-BI plays a crucial role in cholesterol metabolism and reverse cholesterol transport.
Purpose of the Study:
- To investigate the effect of low-dose aspirin on SR-BI expression in human atherosclerotic plaques.
- To elucidate the role of nuclear factor-kappa B (NF-kappaB) in aspirin-mediated SR-BI regulation.
Main Methods:
- Comparison of SR-BI and CD68 expression in carotid atherosclerotic specimens from patients with or without aspirin medication.
- In vitro studies using human THP-1-derived macrophages and primary macrophages from NF-kappaB/p50 knockout mice.
- In vivo studies in NF-kappaB/p50 knockout mice treated with aspirin.
Main Results:
- Aspirin significantly increased SR-BI protein expression in human atherosclerotic plaques.
- Aspirin did not affect CD68 expression, indicating no change in macrophage content.
- Aspirin-induced SR-BI expression was dependent on NF-kappaB signaling, as shown by abrogation in NF-kappaB inhibited cells and NF-kappaB/p50 knockout mice.
Conclusions:
- Aspirin treatment enhances SR-BI expression in human plaque macrophages.
- The effect of aspirin on SR-BI is mediated through the NF-kappaB pathway.
- These findings suggest a potential mechanism for aspirin's cardiovascular benefits involving cholesterol efflux.
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