Hong Chengcheng, Shen Chen, Ding Hongmei, Huang Shanshan, Mu Yun, Su Huihui, Wei Wei, Ma Jun, Zheng Fang
Department of Clinical Immunology, School of Medical Laboratory, Tianjin Medical University, 300203 Tianjin, China.
Departmemt of Medical Laboratory, Jining No.1 People's Hospital, 272011 Shandong Province, China.
Mol Immunol. 2015 Aug;66(2):340-5. doi: 10.1016/j.molimm.2015.03.254. Epub 2015 May 1.
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.
血清淀粉样蛋白A（SAA）在自身免疫性疾病如类风湿关节炎（RA）中已有高表达的报道。然而，SAA在RA发病机制中诱导的详细分子机制仍不清楚。在此，我们聚焦于SAA - SR - B1介导的p38丝裂原活化蛋白激酶（MAPK）信号通路在RA血管生成过程中的作用。我们的结果表明，SAA和SR - B1主要定位于RA滑膜中血管内皮细胞、内衬层和亚内衬层。在一系列用人脐静脉内皮细胞（HUVECs）进行的体外实验中，SAA诱导内皮细胞（ECs）增殖、迁移和管腔形成。然而，阻断SR - B1和p38 MAPK可抑制SAA诱导的细胞增殖、迁移和管腔形成。总之，我们的数据显示了SAA - SR - B1通过p38 MAPK信号通路诱导血管生成事件的一种可能分子机制。
