Neointima formation in a restenosis model is suppressed in midkine- deficient mice

Mitsuru Horiba, Kenji Kadomatsu, Eishin Nakamura, Hisako Muramatsu, Shinya Ikematsu, Sadatoshi Sakuma, Kenji Hayashi, Yukio Yuzawa, Seiichi Matsuo, Masafumi Kuzuya, Tadashi Kaname, Makoto Hirai, Hidehiko Saito, Takashi Muramatsu

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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. These results indicate that MK plays a critical role in neointima formation at least in part owing to its ability to mediate leukocyte recruitment.

Original languageEnglish
Pages (from-to)489-495
Number of pages7
JournalJournal of Clinical Investigation
Volume105
Issue number4
DOIs
Publication statusPublished - 02-2000

All Science Journal Classification (ASJC) codes

  • Medicine(all)

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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. (2000). Neointima formation in a restenosis model is suppressed in midkine- deficient mice. Journal of Clinical Investigation, 105(4), 489-495. https://doi.org/10.1172/JCI7208