An involvement of SR-B1 mediated p38 MAPK signaling pathway in serum amyloid A-induced angiogenesis in rheumatoid arthritis

Chengcheng Hong; Chen Shen; Hongmei Ding; Shanshan Huang; Yun Mu; Huihui Su; Wei Wei; Jun Ma; Fang Zheng

doi:10.1016/j.molimm.2015.03.254

An involvement of SR-B1 mediated p38 MAPK signaling pathway in serum amyloid A-induced angiogenesis in rheumatoid arthritis

Mol Immunol. 2015 Aug;66(2):340-5. doi: 10.1016/j.molimm.2015.03.254. Epub 2015 May 1.

Authors

Chengcheng Hong¹, Chen Shen², Hongmei Ding¹, Shanshan Huang¹, Yun Mu³, Huihui Su¹, Wei Wei⁴, Jun Ma⁵, Fang Zheng⁶

Affiliations

¹ Department of Clinical Immunology, School of Medical Laboratory, Tianjin Medical University, 300203 Tianjin, China.
² Departmemt of Medical Laboratory, Jining No.1 People's Hospital, 272011 Shandong Province, China.
³ Department of Medical Laboratory, Tianjin Children's Hospital, 300074 Tianjin, China.
⁴ Department of Rheumatology, General Hospital, Tianjin Medical University, 300052 Tianjin, China.
⁵ Department of Health Statistics, College of Public Health, Tianjin Medical University, 300203, Tianjin, China. Electronic address: majun@tmu.edu.cn.
⁶ Department of Clinical Immunology, School of Medical Laboratory, Tianjin Medical University, 300203 Tianjin, China. Electronic address: fangzheng@tmu.edu.cn.

PMID: 25932604
DOI: 10.1016/j.molimm.2015.03.254

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.

Keywords: Angiogenesis; Rheumatoid arthritis; Scavenger Receptor Class B Type 1; Serum amyloid A; p38 MAPK.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Arthritis, Rheumatoid / genetics
Arthritis, Rheumatoid / immunology*
Arthritis, Rheumatoid / pathology
Cell Movement
Cell Proliferation
Cells, Cultured
Gene Expression Regulation
Human Umbilical Vein Endothelial Cells / cytology
Human Umbilical Vein Endothelial Cells / drug effects
Human Umbilical Vein Endothelial Cells / immunology
Humans
Neovascularization, Pathologic / chemically induced
Neovascularization, Pathologic / immunology*
Neovascularization, Pathologic / pathology
Osteoarthritis / genetics
Osteoarthritis / immunology*
Osteoarthritis / pathology
Scavenger Receptors, Class B / chemistry
Scavenger Receptors, Class B / immunology*
Serum Amyloid A Protein / immunology
Serum Amyloid A Protein / pharmacology*
Signal Transduction
Synovial Membrane / drug effects*
Synovial Membrane / immunology
Synovial Membrane / pathology
p38 Mitogen-Activated Protein Kinases / genetics
p38 Mitogen-Activated Protein Kinases / immunology*

Substances

SCARB1 protein, human
Scavenger Receptors, Class B
Serum Amyloid A Protein
p38 Mitogen-Activated Protein Kinases