biostudies-literatureUnknown105(4)Horiba MNeointima 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. TThe Journal of clinical investigation489-95https://www.ebi.ac.uk/biostudies/studies/S-EPMC289157biostudies-literatureNeointima formation in a restenosis model is suppressed in midkine-deficient mice.PMC289157Kaname TSakuma SHirai MNakamura EHoriba MHayashi KKuzuya MKadomatsu KMatsuo SMuramatsu TSaito HMuramatsu HYuzawa YIkematsu SfalseNeointima formation in a restenosis model is suppressed in midkine-deficient mice.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. T2000-01-01T00:00:00Z2000 Feb2025-04-26T04:25:35.432Z2019-03-27T00:36:03ZS-EPMC2891571068337810.1172/JCI7208