{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["105(4)"],"submitter":["Horiba M"],"pubmed_abstract":["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. T"],"journal":["The Journal of clinical investigation"],"pagination":["489-95"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC289157"],"repository":["biostudies-literature"],"pubmed_title":["Neointima formation in a restenosis model is suppressed in midkine-deficient mice."],"pmcid":["PMC289157"],"pubmed_authors":["Kaname T","Sakuma S","Hirai M","Nakamura E","Horiba M","Hayashi K","Kuzuya M","Kadomatsu K","Matsuo S","Muramatsu T","Saito H","Muramatsu H","Yuzawa Y","Ikematsu S"],"additional_accession":[]},"is_claimable":false,"name":"Neointima formation in a restenosis model is suppressed in midkine-deficient mice.","description":"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. T","dates":{"release":"2000-01-01T00:00:00Z","publication":"2000 Feb","modification":"2025-04-26T04:25:35.432Z","creation":"2019-03-27T00:36:03Z"},"accession":"S-EPMC289157","cross_references":{"pubmed":["10683378"],"doi":["10.1172/JCI7208"]}}