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Journal of Biochemistry Advance Access published online on January 29, 2009
Journal of Biochemistry, doi:10.1093/jb/mvp021
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© The authors 2009. Published by Oxford University Press on behalf of the Japanese Biochemical Society. All rights reserved.

Induction and expression of anti-angiogenic vasohibins in the hematopoietic stem/progenitor cell population

Hisamichi Naito1, Hiroyasu Kidoya1, Yasufumi Sato2 and Nobuyuki Takakura1,*

From 1 the Department of Signal Transduction, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamada-oka, Suita-shi, Osaka 565-0871, Japan, 2 Department of Vascular Biology, Institute of Development, Aging, and Cancer, Tohoku University, 4-1 Seiryo-machi, Aoba-ku, Sendai 980-8575, Japan.

*To whom correspondence should be addressed: Nobuyuki Takakura: Tel: +81-6-6879-8316. Fax: +81-6-6879-8314. E-mail: ntakaku{at}biken.osaka-u.ac.jp

Received January 8, 2009; Accepted January 23, 2009


  Abstract

Hematopoiesis and blood vessel formation are closely associated, with several molecules employed by both systems. Recently, vasohibin-1 (VASH1), an endothelium-derived negative feedback regulator of angiogenesis, has been isolated and characterized. VASH1 is induced by VEGF or bFGF in endothelial cells (ECs) and inhibits their proliferation and migration. However, there are no data on the induction and expression of VASH1 in hematopoietic cells (HCs). Here, we show that the hematopoietic stem cell (HSC) population, but not hematopoietic progenitors (HPs) or mature HCs from adult bone marrow (BM) constitutively express VASH1. However, HPs but not HSCs can be induced to express VASH1 after BM suppression by 5-FU. Knock-down of the VASH1 gene in VASH1+ leukemia cells induced cell proliferation. These results suggest a role for VASH1 in negative feedback regulation of HP proliferation during recovery following BM ablation.

Key Words: vasohibin, hematopoietic stem cell, hematopoietic progenitor cells, bone marrow ablation, 5-FU


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