2009年5月
Distinctive localization and opposed roles of vasohibin-1 and vasohibin-2 in the regulation of angiogenesis
BLOOD
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- 巻
- 113
- 号
- 19
- 開始ページ
- 4810
- 終了ページ
- 4818
- 記述言語
- 英語
- 掲載種別
- DOI
- 10.1182/blood-2008-07-170316
- 出版者・発行元
- AMER SOC HEMATOLOGY
We recently isolated a novel angiogenesis inhibitor, vasohibin-1, and its homologue, vasohibin-2. In this study we characterize the role of these 2 molecules in the regulation of angiogenesis. In a mouse model of subcutaneous angiogenesis, the expression of endogenous vasohibin-1 was low in proliferating ECs at the sprouting front but high in nonproliferating endothelial cells (ECs) in the termination zone. In contrast, endogenous vasohibin-2 was preferentially expressed in mononuclear cells mobilized from bone marrow that infiltrated the sprouting front. When applied exogenously, vasohibin-1 inhibited angiogenesis at the sprouting front where endogenous vasohibin-1 was scarce but did not influence vascularity in the termination zone where endogenous vasohibin-1 was enriched. Exogenous vasohibin-2 prevented the termination of angiogenesis in the termination zone and increased vascularity in this region. Angiogenesis was persistent in the termination zone in the vasohibin-1 knockout mice, whereas angiogenesis was deficient at the sprouting front in the vasohibin-2 knockout mice. Supplementation of deficient proteins normalized the abnormal patterns of angiogenesis in the vasohibin knockout mice. These results indicate that vasohibin-1 is expressed in ECs in the termination zone to halt angiogenesis, whereas vasohibin-2 is expressed in infiltrating mononuclear cells in the sprouting front to promote angiogenesis. (Blood. 2009;113:4810-4818)
- リンク情報
- ID情報
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- DOI : 10.1182/blood-2008-07-170316
- ISSN : 0006-4971
- Web of Science ID : WOS:000265910300045