Title
Apolipoprotein C-I is crucially involved in lipopolysaccharide-induced atherosclerosis development in apolipoprotein E-knockout mice
Author
TNO Kwaliteit van Leven
Westerterp, M.
Berbée, J.F.P.
Pires, N.M.M.
van Mierlo, G.J.D.
Kleemann, R.
Romijn, J.A.
Havekes, L.M.
Rensen, P.C.N.
Publication year
2007
Abstract
BACKGROUND - Lipopolysaccharide (LPS), which is released from Gram-negative bacteria on multiplication or lysis, aggravates atherosclerosis in humans and rodents by inducing inflammation via toll-like receptors. Because apolipoprotein C-I (apoCI) enhances the LPS-induced inflammatory response in macrophages in vitro and in mice, we investigated the effect of endogenous apoCI expression on LPS-induced atherosclerosis in mice. METHODS AND RESULTS - Twelve-week-old apoeapoc1 and apoeapoc1 mice received weekly intraperitoneal injections of LPS (50 ug) or vehicle for a period of 10 weeks, and atherosclerosis development was assessed in the aortic root. LPS administration did not affect atherosclerotic lesion area in apoeapoc1 mice but increased it in apoeapoc1 mice. In fact, apoCI expression increased the LPS-induced atherosclerotic lesion area by 60% (P
Subject
Biomedical Research
Apolipoproteins
Atherosclerosis
Hypercholesterolemia
Inflammation
Leukocytes
Lipoproteins
apolipoprotein C1
apolipoprotein E
bacterium lipopolysaccharide
endothelial leukocyte adhesion molecule 1
fibrinogen
tumor necrosis factor alpha
animal cell
animal experiment
animal model
animal tissue
aorta atherosclerosis
aorta root
article
atherogenesis
atherosclerosis
bacterial infection
controlled study
female
fibrinogen blood level
inflammation
knockout mouse
macrophage
mouse
nonhuman
priority journal
protein blood level
protein expression
Animals
Apolipoproteins C
Atherosclerosis
Biological Markers
Cells, Cultured
Cholesterol, HDL
E-Selectin
Female
Fibrinogen
Hypercholesterolemia
Lipopolysaccharides
Macrophages, Peritoneal
Male
Mice
Mice, Inbred C57BL
Mice, Mutant Strains
Monocytes
T-Lymphocytes
Tumor Necrosis Factor-alpha
Vasculitis
To reference this document use:
http://resolver.tudelft.nl/uuid:5a8789b4-29bf-4a79-bd37-6f1e80b81e73
DOI
https://doi.org/10.1161/circulationaha.107.693382
TNO identifier
240260
ISSN
0009-7322
Source
Circulation, 116 (116), 2173-2181
Document type
article