An involvement of SR-B1 mediated p38 MAPK signaling pathway in serum amyloid A-induced angiogenesis in rheumatoid arthritis. Issue 2 (August 2015)

• Record Type: Journal Article
• Authors: Hong, Chengcheng; Shen, Chen; Ding, Hongmei; Huang, Shanshan; Mu, Yun; Su, Huihui; Wei, Wei; Ma, Jun; Zheng, Fang
• Is Part Of: Molecular immunology. Volume 66:Issue 2(2015:Aug.)
• Page Start: 340
• Page End: 345
• Publication Date: 2015-08
• Subjects: Serum amyloid A -- Scavenger Receptor Class B Type 1 -- Rheumatoid arthritis -- p38 MAPK -- Angiogenesis; SAA serum amyloid A -- SR-B1 scavenger Receptor Class B Type 1 -- RA rheumatoid arthritis -- p38 MAPK p38 mitogen-activated protein kinase -- FPRL1 formyl peptide receptor-like 1 -- TLR2 toll like receptor 2; Immunochemistry -- Periodicals; Molecular biology -- Periodicals; Immunochemistry -- Periodicals; Allergy and Immunology -- Periodicals; Molecular Biology -- Periodicals; Immunochimie -- Périodiques; Biologie moléculaire -- Périodiques; Immunochemistry; Molecular biology; Periodicals; Electronic journals; 571.96
• DOI: 10.1016/j.molimm.2015.03.254
• Languages: English
• ISSNs: 0161-5890

Abstract

Highlights: Localized expression of SAA and SR-B1 in RA synovium was highly present. SAA-induced cell growth, migration and angiogenesis were mediated through SR-B1. SAA activated p38 MAPK signaling pathway involved in angiogenic process of RA. Abstract: Serum amyloid A (SAA) has been reported high expression in autoimmune diseases, such as rheumatoid arthritis (RA). However, detailed molecular mechanisms induced by SAA in the pathogenesis of RA are still unclear. Herein, we focused on the role of SAA–SR-B1 mediated p38 MAPK signaling pathway in the process of RA angiogenesis. Our results showed that both SAA and SR-B1 predominantly localized to vascular endothelial cells, lining and sublining layers in RA synovium. In a series of in vitro experiments with human umbilical vein endothelial cells (HUVECs), SAA induced the endothelial cells (ECs) proliferation, migration and tube formation. However, blockage of SR-B1 and p38 MAPK inhibited SAA-induced cells proliferation, migration and tube formation. In conclusion, our data showed a possible molecular mechanism for SAA–SR-B1 induced angiogenesis events via p38 MAPK signaling pathway.