Serum amyloid A promotes the inflammatory response via p38-MAPK/SR-BI pathway in THP-1 macrophages.
- Author:
Ming-Yan ZHU
1
;
Yan WANG
2
;
Yu WANG
3
;
Feng-Ling PENG
1
;
Han-Xiao OU
1
;
Xiang ZHENG
1
;
Jin-Feng SHI
1
;
Gao-Feng ZENG
4
;
Zhong-Cheng MO
5
Author Information
1. Department of Histology and Embryology, University of South China, Hengyang 421001, China.
2. Department of Anesthesiology, the Second Affiliated Hospital of University of South China, Hengyang 421001, China.
3. Department of Clinical Laboratory, the Second Affiliated Hospital of University of South China, Hengyang 421001, China.
4. Department of Cardiovascular Medicine, the Second Affiliated Hospital of University of South China, Hengyang 421001, China.
5. Department of Histology and Embryology, University of South China, Hengyang 421001, China. zhchmo@hotmail.com.
- Publication Type:Journal Article
- MeSH:
Cell Line;
Chemokine CCL2;
Humans;
Inflammation;
Interleukin-1beta;
MAP Kinase Signaling System;
Macrophages;
Phosphorylation;
Serum Amyloid A Protein;
Tumor Necrosis Factor-alpha;
p38 Mitogen-Activated Protein Kinases
- From:
Acta Physiologica Sinica
2016;68(3):293-300
- CountryChina
- Language:Chinese
-
Abstract:
To investigate the effect and mechanism of serum amyloid A (SAA) on the expression of scavenger receptor class B type I (SR-BI) and inflammatory response in THP-1 macrophages, the human THP-1 cells were treated with SAA and p38-MAPK agonist (anisomycin) or p38-MAPK inhibitor (SB203580). Then, the expressions of SR-BI, phosphorylated p38-MAPK and inflammatory factors (MCP-1, TNF-α, IL-1β) were examined by real-time quantitative PCR, Western blotting and ELISA, respectively. The results showed that, compared with control group, SAA increased the levels of inflammatory factors (MCP-1, TNF-α, IL-1β), down-regulated the expressions of SR-BI, and up-regulated the expression of phosphorylated p38-MAPK protein in a concentration- and time-dependent manner in THP-1 cells (P < 0.05). After treatment with SAA and p38-MAPK agonist (anisomycin) in THP-1 cells, the expression of SR-BI was down-regulated, and the levels of inflammatory factors and phosphorylated p38-MAPK protein expression were increased, compared with the group only treated by SAA (P < 0.05). In contrast, the SR-BI expression was up-regulated, whereas inflammatory factors and phosphorylated p38-MAPK protein expressions were decreased after the cells were treated with SAA and p38-MAPK inhibitor (SB203580) (P < 0.05). The results suggest that SAA-promoted inflammatory response in THP-1 macrophages may be through the phosphorylation of p38-MAPK and inhibition of SR-BI expression.
