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

被引：35

作者：

Hong, Chengcheng ^{[1
]}

Shen, Chen ^{[2
]}

Ding, Hongmei ^{[1
]}

Huang, Shanshan ^{[1
]}

Mu, Yun ^{[3
]}

Su, Huihui ^{[1
]}

Wei, Wei ^{[4
]}

Ma, Jun ^{[5
]}

Zheng, Fang ^{[1
]}

机构：

[1] Tianjin Med Univ, Sch Med Lab, Dept Clin Immunol, Tianjin 300203, Peoples R China

[2] Jining 1 Peoples Hosp, Dept Lab Med, Jining 272011, Shandong, Peoples R China

[3] Tianjin Childrens Hosp, Dept Lab Med, Tianjin 300074, Peoples R China

[4] Tianjin Med Univ, Gen Hosp, Dept Rheumatol, Tianjin 300052, Peoples R China

[5] Tianjin Med Univ, Coll Publ Hlth, Dept Hlth Stat, Tianjin 300203, Peoples R China

来源：

MOLECULAR IMMUNOLOGY | 2015年 / 66卷 / 02期

关键词：

Serum amyloid A; Scavenger Receptor Class B Type 1; Rheumatoid arthritis; p38; MAPK; Angiogenesis; ACTIVATION; EXPRESSION; ASSOCIATION; MIGRATION; BINDING; TISSUE; GENES;

D O I：

10.1016/j.molimm.2015.03.254

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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. (C) 2015 Elsevier Ltd. All rights reserved.

引用

页码：340 / 345

页数：6

共 30 条

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