An involvement of SR-B1 mediated p38 MAPK signaling pathway in serum amyloid A-induced angiogenesis in rheumatoid arthritis.
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.
Department of Clinical Immunology, School of Medical Laboratory, Tianjin Medical University, 300203 Tianjin, China.
Chengcheng
C
Hong
Departmemt of Medical Laboratory, Jining No.1 People's Hospital, 272011 Shandong Province, China.
Chen
C
Shen
Department of Clinical Immunology, School of Medical Laboratory, Tianjin Medical University, 300203 Tianjin, China.
Hongmei
H
Ding
Department of Clinical Immunology, School of Medical Laboratory, Tianjin Medical University, 300203 Tianjin, China.
Shanshan
S
Huang
Department of Medical Laboratory, Tianjin Children's Hospital, 300074 Tianjin, China.
Yun
Y
Mu
Department of Clinical Immunology, School of Medical Laboratory, Tianjin Medical University, 300203 Tianjin, China.
Huihui
H
Su
Department of Rheumatology, General Hospital, Tianjin Medical University, 300052 Tianjin, China.
Wei
W
Wei
Department of Health Statistics, College of Public Health, Tianjin Medical University, 300203, Tianjin, China. Electronic address: majun@tmu.edu.cn.
Jun
J
Ma
Department of Clinical Immunology, School of Medical Laboratory, Tianjin Medical University, 300203 Tianjin, China. Electronic address: fangzheng@tmu.edu.cn.
Fang
F
Zheng
D001172:Arthritis, Rheumatoid / Q000235:genetics / Q000276:immunology* / Q000473:pathology; D002465:Cell Movement; D049109:Cell Proliferation; D002478:Cells, Cultured; D005786:Gene Expression Regulation; D061307:Human Umbilical Vein Endothelial Cells / Q000166:cytology / Q000187:drug effects / Q000276:immunology; D006801:Humans; D009389:Neovascularization, Pathologic / Q000139:chemically induced / Q000276:immunology* / Q000473:pathology; D010003:Osteoarthritis / Q000235:genetics / Q000276:immunology* / Q000473:pathology; D051122:Scavenger Receptors, Class B / Q000737:chemistry / Q000276:immunology*; D000685:Serum Amyloid A Protein / Q000276:immunology / Q000494:pharmacology*; D015398:Signal Transduction; D013583:Synovial Membrane / Q000187:drug effects* / Q000276:immunology / Q000473:pathology; D048051:p38 Mitogen-Activated Protein Kinases / Q000235:genetics / Q000276:immunology*
C495124:SCARB1 protein, human; D051122:Scavenger Receptors, Class B; D000685:Serum Amyloid A Protein; D048051:p38 Mitogen-Activated Protein Kinases
Angiogenesis; Rheumatoid arthritis; Scavenger Receptor Class B Type 1; Serum amyloid A; p38 MAPK