title: Influence of aspirin on SR-BI expression in human carotid plaques.
abstract: 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.
authors.affiliation: Department of Internal Medicine, Innsbruck Medical University, Anichstrasse 35, Innsbruck, Austria.
authors.forename: Andreas
authors.initials: A
authors.lastname: Wehinger
authors.forename: Ivan
authors.initials: I
authors.lastname: Tancevski
authors.forename: Ruediger
authors.initials: R
authors.lastname: Seiler
authors.forename: Sandra M
authors.initials: SM
authors.lastname: Frotschnig
authors.forename: Stefan
authors.initials: S
authors.lastname: Frantz
authors.forename: Julia
authors.initials: J
authors.lastname: Huber
authors.forename: Philipp
authors.initials: P
authors.lastname: Eller
authors.forename: Wilfried
authors.initials: W
authors.lastname: Schgoer
authors.forename: Bernhard
authors.initials: B
authors.lastname: Foeger
authors.forename: Josef R
authors.initials: JR
authors.lastname: Patsch
authors.forename: Andreas
authors.initials: A
authors.lastname: Ritsch
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000096:biosynthesis; D015214:Antigens, Differentiation, Myelomonocytic / Q000096:biosynthesis; D001241:Aspirin / Q000627:therapeutic use*; D050197:Atherosclerosis / Q000188:drug therapy / Q000235:genetics / Q000378:metabolism*; D018955:CD36 Antigens / Q000096:biosynthesis / Q000235:genetics*; D002340:Carotid Artery Diseases / Q000188:drug therapy / Q000378:metabolism*; D016894:Endarterectomy, Carotid; D006801:Humans; D008264:Macrophages / Q000187:drug effects; D051379:Mice; D018345:Mice, Knockout; D016328:NF-kappa B / Q000502:physiology; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D001241:Aspirin; D018955:CD36 Antigens; D016328:NF-kappa B; C067980:CD68 antigen, human; D000097382:CD68 Molecule