| First Author | Cheng G | Year | 2018 |
| Journal | Int Immunopharmacol | Volume | 62 |
| Pages | 203-211 | PubMed ID | 30015240 |
| Mgi Jnum | J:282611 | Mgi Id | MGI:6383325 |
| Doi | 10.1016/j.intimp.2018.06.018 | Citation | Cheng G, et al. (2018) ZIP8 induces monocyte adhesion to the aortas ex-vivo by regulating zinc influx. Int Immunopharmacol 62:203-211 |
| abstractText | Monocytes recruited and adhering to the inflamed arteries are crucial for atherosclerosis development. Here, we report the role of zinc (Zn(2+)) homeostasis in monocyte adhesion and recruitment. By comparing the expression levels of Zn(2+) transporters between non-adhering and adhering monocytes, we found that the Zn(2+) importer ZIP8 was specifically upregulated in monocytes adhering to the aortas ex-vivo. Although the overexpression of ZIP8 increased the absorption of Zn(2+), Fe(2+) and Cd(2+) in monocytes, only Zn(2+) supplementation was demonstrated capable of promoting the adhesion of monocytes to endothelial monolayers in vitro. In addition, we confirmed the role of ZIP8-dependent Zn(2+) influx in promoting monocyte adhesion to the aortas ex-vivo. More importantly, the enforced expression of ZIP8 increased monocyte adhesion and recruitment to the nascent atherosclerotic lesions in ApoE(-/-) mice. Overall, our results suggest that the Zn(2+) influx in monocytes regulated by ZIP8 is a novel factor determining their adhesion and recruitment to atherosclerotic lesions, and that targeting ZIP8 or Zn(2+) homeostasis may represent a novel strategy to interfere these activities. |
