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Egfl7 knockdown causes defects in the extension and junctional arrangements of endothelial cells during zebrafish vasculogenesis
Author(s) -
De Mazière Ann,
Parker Leon,
Van Dijk Suzanne,
Ye Weilan,
Klumperman Judith
Publication year - 2008
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.21441
Subject(s) - vasculogenesis , biology , zebrafish , dorsal aorta , microbiology and biotechnology , gene knockdown , anatomy , lumen (anatomy) , mesoderm , blood vessel , haematopoiesis , embryonic stem cell , stem cell , endocrinology , genetics , cell culture , gene , progenitor cell
The endothelial cell (EC) ‐specific secreted protein EGFL7 is important for tubulogenesis in newly forming blood vessels. We studied its role in vascular tube formation by a quantitative ultrastructural analysis of Egfl7 ‐knockdown zebrafish embryos. At 24 hours postfertilization, the endothelia of dorsal aorta (DA) and posterior cardinal vein (PCV) were correctly anchored to the hypochord and endoderm, respectively, but failed to expand into the vascular area. This resulted in vessels with reduced or split lumen and open sheets of ECs. Concomitantly, the organization of hematopoietic cells—identified by the presence of previously undescribed membrane tubules—between DA and PCV, and within the vessels, was severely disturbed. Strikingly, ectopic cell junctions occurred across the obstructed vessel lumen, on the luminal EC surfaces, which in control conditions never display junctions of any kind. These data suggest that Egfl7 provides ECs with a cue for their extension into the vascular area and in establishing EC cell polarity. Developmental Dynamics 237:580–591, 2008. © 2008 Wiley‐Liss, Inc.