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The Vasohibin Family 英文参考文献
Pharmaceuticals 2010, 3, 433-440; doi:10.3390/ph3020433
OPEN ACCESS
pharmaceuticals
ISSN 1424-8247
/journal/pharmaceuticals
Review
The Vasohibin Family
Yasufumi Sato
Department of Vascular Biology, Institute of Development, Aging and Cancer, Tohoku University,
4-1 Seiryo-machi, Aoba-ku, Sendai 980-8575, Japan; E-Mail: y-sato@idac.tohoku.ac.jp;
Tel.: +81-22-717-8528; Fax: +81-22-717-8533
Received: 13 January 2010; in revised form: 23 January 2010 / Accepted: 3 February 2010 /
Published: 5 February 2010
Abstract: Angiogenesis is regulated by the local balance between angiogenesis stimulators
and inhibitors. A number of endogenous angiogenesis inhibitors have been found in the
body. The origin of these inhibitors is mostly extrinsic to the vasculature. Recently,
however, vascular endothelial cells themselves have been found to produce angiogenesis
inhibitors including vasohibin-1. These intrinsic inhibitors are thought to regulate
angiogenesis by an auto-regulatory or negative-feedback mechanism. This review will focus
on vasohibin-1 produced by vascular endothelial cells and on its homologue, vasohibin-2.
Keywords: endothelial cell; negative feedback; mononuclear cell; bone marrow
1. Introduction
The vasculature is primarily composed of luminal endothelial cells (ECs) and surrounding mural
cells (smooth muscle cells or pericytes). Coverage by mural cells stabilizes blood vessels. The initial
step of angiogenesis is the extrication of mural cells from endothelial tubes for vascular destabilization.
Subsequently, specialized ECs, the so-called “tip” cells, migrate by extending numerous filopodia,
whereas following ECs, the so-called “stalk” cells, proliferate, causing elongation of the sprouts to
form immature tube-like structures. Finally, redistributed mural cells affix themselves to the newly
formed vessels for vascular restabilization. By this process, ECs stop their prolife
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