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Title: Critical roles for murine Reck in the regulation of vascular patterning and stabilization
Authors: De Almeida, Glícia Maria
Yamamoto, Mako
Morioka, Yoko
Ogawa, Shuichiro
Matsuzaki, Tomoko  kyouindb  KAKEN_id
Noda, Makoto  kyouindb  KAKEN_id  orcid (unconfirmed)
Author's alias: 松﨑, 朋子
野田, 亮
Issue Date: 11-Dec-2015
Publisher: Nature Publishing Group
Journal title: Scientific Reports
Volume: 5
Thesis number: 17860
Abstract: Extracellular matrix (ECM) is known to play several important roles in vascular development, although the molecular mechanisms behind these remain largely unknown. RECK, a tumor suppressor downregulated in a wide variety of cancers, encodes a membrane-anchored matrix-metalloproteinase-regulator. Mice lacking functional Reck die in utero, demonstrating its importance for mammalian embryogenesis; however, the underlying causes of mid-gestation lethality remain unclear. Using Reck conditional knockout mice, we have now demonstrated that the lack of Reck in vascular mural cells is largely responsible for mid-gestation lethality. Experiments using cultured aortic explants further revealed that Reck is essential for at least two events in sprouting angiogenesis; (1) correct association of mural and endothelial tip cells to the microvessels and (2) maintenance of fibronectin matrix surrounding the vessels. These findings demonstrate the importance of appropriate cell-cell interactions and ECM maintenance for angiogenesis and the involvement of Reck as a critical regulator of these events.
Description: A Corrigendum to this article was published on 04 March 2016. This article has been updated.
Rights: This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit
DOI(Published Version): 10.1038/srep17860
PubMed ID: 26658478
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