Influence of aspirin on SR-BI expression in human carotid plaques

BackgroundWe recently showed that aspirin promotes scavenger receptor class-B type I (SR-BI) protein expression invitro in primary human macrophages and invivo in resident peritoneal macrophages of mice.MethodsWe 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.ResultsWe 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-κB). In invitro experiments employing cultured primary macrophages from NF-κB/p50 KO mice, aspirin was not able to influence SR-BI expression. Additionally, no considerable effects on SR-BI expression were observed invivo in resident macrophages of NF-κB/p50 KO mice orally treated with low or high doses of aspirin, respectively.ConclusionsWe 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-κB.