Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
Navigation/Suche
- Forscher*innen
- Institutionen
- Projekte
- Publikationen
- Partner
- Geldgeber
- Ausstattung
- Knowhow
- Forschungsfelder
"Köpfe" der aktuellen Meldungen:
Gewählte Publikation:
SHR Neuro Krebs Kardio Lipid Stoffw Microb
Wehinger, A; Tancevski, I; Seiler, R; Frotschnig, SM; Frantz, S; Huber, J; Eller, P; Schgoer, W; Foeger, B; Patsch, JR; Ritsch, A.
Influence of aspirin on SR-BI expression in human carotid plaques.
Atherosclerosis. 2009; 206(1):234-238
Doi: 10.1016/j.atherosclerosis.2009.01.034
[OPEN ACCESS]
Web of Science
PubMed
FullText
FullText_MUG
- Co-Autor*innen der Med Uni Graz
- Eller Philipp
- Altmetrics:
- Dimensions Citations:
- Plum Analytics:
- Scite (citation analytics):
- 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-kappa B). In in vitro experiments employing cultured primary macrophages from NF-kappa B/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-kappa B/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-kappa B. (C) 2009 Elsevier Ireland Ltd. All rights reserved.
- Find related publications in this database (using NLM MeSH Indexing)
- Animals -
- Antigens, CD - biosynthesis
- Antigens, CD36 - biosynthesis Antigens, CD36 - genetics
- Antigens, Differentiation, Myelomonocytic - biosynthesis
- Aspirin - therapeutic use
- Atherosclerosis - drug therapy Atherosclerosis - genetics Atherosclerosis - metabolism
- Carotid Artery Diseases - drug therapy Carotid Artery Diseases - metabolism
- Endarterectomy, Carotid -
- Humans -
- Macrophages - drug effects
- Mice -
- Mice, Knockout -
- NF-kappa B - physiology
- Find related publications in this database (Keywords)
- Aspirin
- SR-BI
- Carotid plaque
- Macrophages
- NF-kappa B
- Atherosclerosis