| First Author | Huang Y | Year | 2012 |
| Journal | Gene | Volume | 498 |
| Issue | 1 | Pages | 91-5 |
| PubMed ID | 22366371 | Mgi Jnum | J:183776 |
| Mgi Id | MGI:5319256 | Doi | 10.1016/j.gene.2012.02.006 |
| Citation | Huang Y, et al. (2012) Aberrant expression of FcgammaRIIIA (CD16) contributes to the development of atherosclerosis. Gene 498(1):91-5 |
| abstractText | Previous studies have documented that Fc receptor III A of immunoglobulin G (FcgammaRIIIA, also named CD16) is involved in the development of coronary heart disease (CHD). However, the mechanism responsible for FcgammaRIIIA's in contribution to CHD development remains largely unclear. Herein, we investigated the possible role of FcgammaRIIIA in the development of atherosclerosis. Our results showed that the elevated level of FcgammaRIIIA 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(-/-) mice with characterized atherosclerosis after feeding with high-fat diet for 10weeks. 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 FcgammaRIIIA (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 FcgammaRIIIA or its signaling thus might represent a promising approach for the prevention and treatment of CHD. |
