Abstract | AIM: METHODS: We investigated the effects of LysoPS on the uptake of oxidized low-density lipoprotein ( oxLDL) and the modulation of inflammatory mediators and ER stress utilizing RAW264.7 cells and mouse peritoneal macrophages ( MPMs). RESULTS: We found that LysoPS augmented cholesterol accumulation in both models. Consistent with these findings, LysoPS increased the expression of scavenger receptors (CD36, MSR1, LOX1 and TLR4). Regarding the involvement of these lipids in inflammation, LysoPS significantly decreased the expression of inflammatory mediators in lipopolysaccharide (LPS)-treated RAW264.7 cells and MPMs. LysoPS also attenuated ER stress in LPS-untreated RAW264.7 cells. The expression patterns of LysoPS receptors differed considerably among the LPS-untreated RAW264.7 cells, LPS-treated RAW264.7 cells and MPMs. CONCLUSIONS: LysoPS may have proatherosclerotic properties in the setting of foam cell formation as well as antiatherosclerotic effects on inflammation in macrophages.
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Authors | Masako Nishikawa, Makoto Kurano, Hitoshi Ikeda, Junken Aoki, Yutaka Yatomi |
Journal | Journal of atherosclerosis and thrombosis
(J Atheroscler Thromb)
Vol. 22
Issue 5
Pg. 518-26
( 2015)
ISSN: 1880-3873 [Electronic] Japan |
PMID | 25445889
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Lipopolysaccharides
- Lipoproteins, LDL
- Lysophospholipids
- lysophosphatidylserine
- oxidized low density lipoprotein
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Topics |
- Animals
- Atherosclerosis
(physiopathology)
- Cell Line
- Endoplasmic Reticulum
(metabolism)
- Lipopolysaccharides
(pharmacology)
- Lipoproteins, LDL
(metabolism)
- Lysophospholipids
(physiology)
- Macrophages
(drug effects, metabolism, physiology)
- Mice
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