Linked Life Data

16816107

Source:http://linkedlifedata.com/resource/pubmed/id/16816107

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2006-7-3
pubmed:abstractText
Scavenger receptor class B type I (SR-BI) has been shown to be expressed in human atherosclerotic plaque macrophages, where it is believed to reduce atherosclerosis by promoting cholesterol efflux. In this study we investigated the influence of aspirin and other NSAIDs on SR-BI expression and function in cultured human macrophages as well as in different mouse strains. Incubation of human macrophages with 0.5 mmol/l aspirin resulted in increased SR-BI protein expression and increased uptake of HDL-associated [3H]cholesteryl oleate without changes of SR-BI mRNA levels. In contrast, using 5 mmol/l of aspirin, SR-BI expression and function were significantly decreased. Sodium salicylate exerted similar effects on SR-BI expression, whereas no effects were observed using known COX1/2 inhibitors ibuprofen and naproxen, respectively. In in vivo studies low-dose aspirin treatment (6 mg/kg.day) induced SR-BI expression in wild-type and PPAR-alpha knockout mice, respectively, whereas the opposite effect was observed upon high-dose aspirin treatment (60 mg/kg.day) in these animals. We could show that COX-independent effects of aspirin were able to enhance expression of SR-BI in macrophages in a post-transcriptional, PPAR-alpha independent way, suggesting a novel pharmacologic effect of aspirin.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1530-6860
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
20
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1328-35
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Aspirin regulates expression and function of scavenger receptor-BI in macrophages: studies in primary human macrophages and in mice.
pubmed:affiliation
Department of Internal Medicine, Innsbruck Medical University, Anichstrasse 35, Innsbruck 6020, Austria.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't