PubMed ID MGI Ref. ID | Title | Curated Data | Vol(Iss)Pg | ||||
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Horiba M; Kadomatsu K; Nakamura E; Muramatsu H; Ikematsu S; Sakuma S; Hayashi K; Yuzawa Y; Matsuo S; Kuzuya M; Kaname T; Hirai M; Saito H; Muramatsu T | Neointima formation in a restenosis model is suppressed in midkine-deficient mice. | J Clin Invest | 2000 | 105 (4) 489-95 | 5.592828 | ||
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. |
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO) |
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last database update 12/17/2024 MGI 6.24 |
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