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.
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 humanTHP-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: Francesco Cipollone; Andrea Mezzetti; Maria Luigia Fazia; Chiara Cuccurullo; Annalisa Iezzi; Sante Ucchino; Francesco Spigonardo; Marco Bucci; Franco Cuccurullo; Stephen M Prescott; Diana M Stafforini Journal: Arterioscler Thromb Vasc Biol Date: 2005-06-02 Impact factor: 8.311
Authors: K Hirano; S Yamashita; Y Nakagawa; T Ohya; F Matsuura; K Tsukamoto; Y Okamoto; A Matsuyama; K Matsumoto; J Miyagawa; Y Matsuzawa Journal: Circ Res Date: 1999-07-09 Impact factor: 17.367
Authors: Jihong Han; Michael Parsons; Xiaoye Zhou; Andrew C Nicholson; Antonio M Gotto; David P Hajjar Journal: Circulation Date: 2004-11-22 Impact factor: 29.690
Authors: Y Ji; B Jian; N Wang; Y Sun; M L Moya; M C Phillips; G H Rothblat; J B Swaney; A R Tall Journal: J Biol Chem Date: 1997-08-22 Impact factor: 5.157