title: [Serum amyloid A promotes the inflammatory response via p38-MAPK/SR-BI pathway in THP-1 macrophages].
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.
authors.affiliation: Department of Histology and Embryology, University of South China, Hengyang 421001, China.|Department of Cardiovascular Medicine, the Second Affiliated Hospital of University of South China, Hengyang 421001, China.
authors.forename: Ming-Yan
authors.initials: MY
authors.lastname: Zhu
authors.affiliation: Department of Anesthesiology, the Second Affiliated Hospital of University of South China, Hengyang 421001, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Department of Clinical Laboratory, the Second Affiliated Hospital of University of South China, Hengyang 421001, China.
authors.forename: Yu
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Department of Histology and Embryology, University of South China, Hengyang 421001, China.
authors.forename: Feng-Ling
authors.initials: FL
authors.lastname: Peng
authors.affiliation: Department of Histology and Embryology, University of South China, Hengyang 421001, China.
authors.forename: Han-Xiao
authors.initials: HX
authors.lastname: Ou
authors.affiliation: Department of Histology and Embryology, University of South China, Hengyang 421001, China.
authors.forename: Xiang
authors.initials: X
authors.lastname: Zheng
authors.affiliation: Department of Histology and Embryology, University of South China, Hengyang 421001, China.
authors.forename: Jin-Feng
authors.initials: JF
authors.lastname: Shi
authors.affiliation: Department of Cardiovascular Medicine, the Second Affiliated Hospital of University of South China, Hengyang 421001, China.
authors.forename: Gao-Feng
authors.initials: GF
authors.lastname: Zeng
authors.affiliation: Department of Histology and Embryology, University of South China, Hengyang 421001, China. zhchmo@hotmail.com.
authors.forename: Zhong-Cheng
authors.initials: ZC
authors.lastname: Mo
mesh_terms: D002460:Cell Line; D018932:Chemokine CCL2; D006801:Humans; D007249:Inflammation; D053583:Interleukin-1beta; D020935:MAP Kinase Signaling System; D008264:Macrophages; D010766:Phosphorylation; D000685:Serum Amyloid A Protein; D014409:Tumor Necrosis Factor-alpha; D048051:p38 Mitogen-Activated Protein Kinases
chemical_list: C111835:CCL2 protein, human; D018932:Chemokine CCL2; D053583:Interleukin-1beta; D000685:Serum Amyloid A Protein; D014409:Tumor Necrosis Factor-alpha; D048051:p38 Mitogen-Activated Protein Kinases