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See article by Yoshioka et al. [6] (pages 61–69) in this issue . It is a generally accepted view that endothelial damage triggers the pathogenesis of various types of vascular diseases [1]. A growing body of evidence suggests that bone marrow (BM)-derived cells may participate in arterial repair after injury [2,3] by homing to the injured vessel and differentiating into endothelial cells (ECs). Walter et al. suggested that the mobilization of endothelial progenitor cells (EPCs) from BM after vascular injury may mediate accelerated reendothelialization and reduced neointima formation by statin therapy [4]. It was reported that granulocyte colony-stimulating factor (G-CSF), a major regulator of haemopoiesis and the innate immune system, potently mobilizes EPCs from BM and accelerates reendothelialization [5]. In the current issue of Cardiovascular Research , Yoshioka et al. examined a hypothesis that G-CSF treatment could reduce neointimal formation by increasing the number of circulating EPCs and thereby accelerating reendothelialization after mechanical vascular injury [6]. Pre-treatment with G-CSF before the vascular injury enhanced reendothelialization and decreased neointimal formation. These favourable effects on the injured artery were associated with an increase in the number of putative EPCs (CD34+ Flk-1+ cells) in peripheral blood and a decrease in serum IL-6 level. To assess the effective contribution of EPCs originating from the BM itself, the investigators replaced the BM cells of wild-type mice with those from GFP- or Tie-2/LacZ-transgenic mice and … * Corresponding author. Department of Cardiovascular Medicine, University of Tokyo, Graduate School of Medicine, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan. Tel.: +81 3 3815 5411; fax: +81 3 3814 0021. Email address: msata-circ{at}umin.ac.jp |
