Click here to close Hello! We notice that you are using Internet Explorer, which is not supported by Xenbase and may cause the site to display incorrectly. We suggest using a current version of Chrome, FireFox, or Safari.
Biochem Biophys Res Commun January 1, 2020; 521 (4): 907-913.
Show Gene links Show Anatomy links

Adamts18 deficiency in zebrafish embryo causes defective trunk angiogenesis and caudal vein plexus formation.

Lu T , Zhang T , Wang C , Yang N , Pan YH , Dang S , Zhang W .

ADAMTS (A Disintegrin and Metalloproteinase with Thrombospondin type I motifs) enzymes play an important role in various morphogenesis processes. To determine the functions of Adamts18 in the early stages of organogenesis, we created Adamts18 deficient zebrafish using morpholino antisense oligonucleotides (MO) to generate exon 3 skipped adamts18 mRNA transcripts. Results showed that Adamts18 deficiency in zebrafish embryos caused developmental defects, including expanded brain ventricle and hindbrain edema, eye defects, and accumulation of blood in the caudal vein. Adamts18 deficiency also led to impaired trunk angiogenesis and formation of the caudal vein plexus (CVP). Consequently, Adamts18 deficient zebrafish embryos exhibited incomplete formation of intersegment vessels (ISVs), disruption of the honeycomb structure of CVP, and reduced CVP area and loop number. Furthermore, Adamts18 deficiency resulted in impaired blood circulation in major trunk, caudal vein (CV), and common cardinal vein (CCV). These aberrant vascular phenotypes in mutant zebrafish embryos were shown to be associated with a decreased expression of multiple angiogenesis-related signaling genes, including slit/robo, dll4/Notch, cox2, and fgfr. These findings indicate the critical role of Adamts18 in the early stages of vascular network development.

PubMed ID: 31711643
Article link: Biochem Biophys Res Commun

Species referenced: Xenopus
Genes referenced: adam28.2 adamts18 cox2 ptgs2