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

نویسندگان

  • M Horiba
  • K Kadomatsu
  • E Nakamura
  • H Muramatsu
  • S Ikematsu
  • S Sakuma
  • K Hayashi
  • Y Yuzawa
  • S Matsuo
  • M Kuzuya
  • T Kaname
  • M Hirai
  • H Saito
  • T Muramatsu
چکیده

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.

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عنوان ژورنال:
  • The Journal of clinical investigation

دوره 105 4  شماره 

صفحات  -

تاریخ انتشار 2000