| First Author | Horiba M | Year | 2000 |
| Journal | J Clin Invest | Volume | 105 |
| Issue | 4 | Pages | 489-95 |
| PubMed ID | 10683378 | Mgi Jnum | J:60666 |
| Mgi Id | MGI:1353777 | Doi | 10.1172/JCI7208 |
| Citation | Horiba M, et al. (2000) Neointima formation in a restenosis model is suppressed in midkine-deficient mice. J Clin Invest 105(4):489-95 |
| abstractText | Neointima formation is a common feature of atherosclerosis and restenosis after balloon angioplasty. To find a new target to suppress neointima formation, we investigated the possible role of midkine (MK), a heparin-binding growth factor with neurotrophic and chemotactic activities, in neointima formation. MK expression increased during neointima formation caused by intraluminal balloon injury of the rat carotid artery. Neointima formation in a restenosis model was strongly suppressed in MK-deficient mice. Continuous administration of MK protein to MK-deficient mice restored neointima formation. Leukocyte recruitment to the vascular walls after injury was markedly decreased in MK-deficient mice. Soluble MK as well as that bound to the substratum induced migration of macrophages in vitro. These results indicate that MK plays a critical role in neointima formation at least in part owing to its ability to mediate leukocyte recruitment. |
