Aberrant expression of Fc纬RIIIA (CD16) contributes to the development of atherosclerosis
- 作者：Ye Huang ; Huijun Yin ; huijunyin@yahoo.com.cn ; Jingshang Wang ; Qian Liu ; Caifeng Wu ; Keji Chen
- 关键词：Fc纬RIIIA ; Fc receptor III A of immunoglobulin G ; HUVECs ; human umbilical vein endothelial cells ; CHD ; coronary heart disease ; Sm ; simvastatin ; M-CSF ; macrophage colony stimulating factor ; IVIG ; intravenous immunoglobulin ; MFI ; mean fluorescent intensity
- 刊名：Gene
- 出版年：2012
- 期刊代码：73_03781119
- 类别：bio
- 出版时间：25 April, 2012
- 卷：498
- 期：1
- 页码：91-95
- 文件大小：709 K
摘要
Previous studies have documented that Fc receptor III A of immunoglobulin G (Fc纬RIIIA, also named CD16) is involved in the development of coronary heart disease (CHD). However, the mechanism responsible for Fc纬RIIIA's in contribution to CHD development remains largely unclear. Herein, we investigated the possible role of Fc纬RIIIA in the development of atherosclerosis. Our results showed that the elevated level of Fc纬RIIIA on monocytes closely correlated to the adhesive efficiency of human umbilical vein endothelial cells (HUVECs) in vitro. Importantly, we also observed increased population of CD16+ monocytes and elevated CD16 level on monocytes in ApoE鈭?鈭?/sup> mice with characterized atherosclerosis after feeding with high-fat diet for 10 weeks. The enhancement of CD16 on monocytes closely correlated to increased content of MMP-9 in aorta and increased inflammatory cytokines in sera. In addition, similar to simvastatin, recombinant human M-CSF represented a robust inhibitory influence on plaque instability and inflammation. Taken together, these data established that Fc纬RIIIA (CD16)-mediated signaling orchestrated by interaction between monocytes and HUVECs, coupled with inflammatory cytokine stimulation and MMP activation, as a fundamental pathway linked to the development of atherosclerotic formation. Inhibition of Fc纬RIIIA or its signaling thus might represent a promising approach for the prevention and treatment of CHD.