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ZFIN ID: ZDB-PUB-150716-3
Betaglycan knock-down causes embryonic angiogenesis defects in zebrafish
Kamaid, A., Molina-Villa, T., Mendoza, V., Pujades, C., Maldonado, E., Ispizua Belmonte, J.C., López-Casillas, F.
Date: 2015
Source: Genesis (New York, N.Y. : 2000) 53(9): 583-603 (Journal)
Registered Authors: Maldonado, Ernesto
Keywords: Genetics, Mesoderm, Organogenesis, Vasculature
MeSH Terms: none
PubMed: 26174808 Full text @ Genesis
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ABSTRACT
Angiogenesis is an essential requirement for embryonic development and adult homeostasis. Its deregulation is a key feature of numerous pathologies and many studies have shown that members of the transforming growth factor beta (TGF-β) family of proteins play important roles in angiogenesis during development and disease. Betaglycan (BG), also known as TGF-β receptor type III, is a TGF-β co-receptor essential for mice embryonic development but its role in angiogenesis has not been described. We have cloned the cDNA encoding zebrafish BG, a TGF-β-binding membrane proteoglycan that showed a dynamic expression pattern in zebrafish embryos, including the notochord and cells adjacent to developing vessels. Injection of antisense morpholinos decreased BG protein levels and morphant embryos exhibited impaired angiogenesis that was rescued by co-injection with rat BG mRNA. In vivo time-lapse microscopy revealed that BG deficiency differentially affected arterial and venous angiogenesis: morphants showed impaired pathfinding of intersegmental vessels migrating from dorsal aorta, while endothelial cells originating from the caudal vein displayed sprouting and migration defects. Our results reveal a new role for BG during embryonic angiogenesis in zebrafish, which has not been described in mammals and pose interesting questions about the molecular machinery regulating angiogenesis in different vertebrates.
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