Influence of aspirin on SR-BI expression in human carotid plaques
| Autor: | Ivan Tancevski, Andreas Wehinger, Ruediger Seiler, Josef R. Patsch, Philipp Eller, Sandra Frotschnig, Andreas Ritsch, Bernhard Foeger, Stefan Frantz, Julia M. Huber, Wilfried Schgoer |
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| Rok vydání: | 2009 |
| Předmět: |
CD36 Antigens
Carotid Artery Diseases Antigens Differentiation Myelomonocytic Pharmacology Article Mice Antigens CD In vivo medicine Animals Humans Macrophage Antipyretic Scavenger receptor Mice Knockout Endarterectomy Carotid Aspirin business.industry CD68 Macrophages NF-kappa B Atherosclerosis NFKB1 medicine.anatomical_structure Immunology Cardiology and Cardiovascular Medicine business medicine.drug Blood vessel |
| Zdroj: | Atherosclerosis. 206:234-238 |
| ISSN: | 0021-9150 |
| Popis: | 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 (100mg/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-κB). In in vitro 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 in vivo in resident macrophages of NF-κB/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-κB. |
| Databáze: | OpenAIRE |
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