PUBLICATION
Yap/Taz transcriptional activity is essential for vascular regression via Ctgf expression and actin polymerization
- Authors
- Nagasawa-Masuda, A., Terai, K.
- ID
- ZDB-PUB-170404-7
- Date
- 2017
- Source
- PLoS One 12: e0174633 (Journal)
- Registered Authors
- Terai, Kenta
- Keywords
- Embryos, Zebrafish, Actin polymerization, Angiogenesis, Veins, Aorta, Blood flow, Transcriptional control
- MeSH Terms
-
- Actins/metabolism*
- Animals
- Animals, Genetically Modified
- Cell Line
- Connective Tissue Growth Factor/biosynthesis*
- HEK293 Cells
- Human Umbilical Vein Endothelial Cells/metabolism
- Humans
- In Situ Hybridization
- Morpholinos/genetics
- Neovascularization, Physiologic
- Trans-Activators/genetics
- Trans-Activators/metabolism*
- Transcription Factors/genetics
- Transcription Factors/metabolism*
- Transcriptional Activation/genetics
- Zebrafish/embryology*
- Zebrafish/genetics
- Zebrafish/metabolism*
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism*
- PubMed
- 28369143 Full text @ PLoS One
Citation
Nagasawa-Masuda, A., Terai, K. (2017) Yap/Taz transcriptional activity is essential for vascular regression via Ctgf expression and actin polymerization. PLoS One. 12:e0174633.
Abstract
Vascular regression is essential to remove redundant vessels during the formation of an efficient vascular network that can transport oxygen and nutrient to every corner of the body. However, no mechanism is known to explain how major blood vessels regress during development. Here we use the dorsal part of the caudal vein plexus (dCVP) in Zebrafish to investigate the mechanism of regression and discover a new role of Yap/Taz in vascular regression. During regression, Yap/Taz is activated by blood circulation in the endothelial cells. This leads to induction of Ctgf and actin polymerization. Interference with Yap/Taz activation decreased Ctgf production, which decreased actin polymerization and vascular regression. These results implicate a novel role of Yap/Taz in vascular regression.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping