Serum amyloid A stimulates macrophage foam cell formation via lectin-like oxidized low-density lipoprotein receptor 1 upregulation
- Authors
- Lee, HY[Lee, Ha Young]; Kim, SD[Kim, Sang Doo]; Baek, SH[Baek, Suk-Hwan]; Choi, JH[Choi, Joon Hyuk]; Cho, KH[Cho, Kyung-Hyun]; Zabel, BA[Zabel, Brian A.]; Bae, YS[Bae, Yoe-Sik]
- Issue Date
- 29-Mar-2013
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- Serum amyloid A; Foam cell; Atherosclerosis; Lecti
- Citation
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.433, no.1, pp.18 - 23
- Indexed
- SCIE
SCOPUS
- Journal Title
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
- Volume
- 433
- Number
- 1
- Start Page
- 18
- End Page
- 23
- URI
- https://scholarworks.bwise.kr/skku/handle/2021.sw.skku/61191
- DOI
- 10.1016/j.bbrc.2013.02.077
- ISSN
- 0006-291X
- Abstract
- Elevated levels of serum amyloid A (SAA) is a risk factor for cardiovascular diseases, however, the role of SAA in the pathophysiology of atherosclerosis remains unclear. Here we show that SAA induced macrophage foam cell formation. SAA-stimulated foam cell formation was mediated by c-jun N-terminal kinase (JNK) signaling. Moreover, both SAA and SAA-conjugated high density lipoprotein stimulated the expression of the important scavenger receptor lectin-like oxidized low-density lipoprotein receptor 1 (LOX1) via nuclear factor-kappa B (NF-kappa B). A LOX1 antagonist carrageenan significantly blocked SAA-induced foam cell formation, indicating that SAA promotes foam cell formation via LOX1 expression. Our findings therefore suggest that SAA stimulates foam cell formation via LOX1 induction, and thus likely contributes to atherogenesis. (c) 2013 Elsevier Inc. All rights reserved.
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- Appears in
Collections - Science > Department of Biological Science > 1. Journal Articles
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