PUBLICATION
Ftr82 Is Critical for Vascular Patterning during Zebrafish Development
- Authors
- Chang, H.W., Wang, W.D., Chiu, C.C., Chen, C.H., Wang, Y.S., Chen, Z.Y., Liu, W., Tai, M.H., Wen, Z.H., Wu, C.Y.
- ID
- ZDB-PUB-170119-3
- Date
- 2017
- Source
- International Journal of Molecular Sciences 18(1): (Journal)
- Registered Authors
- Wang, Wen-Der
- Keywords
- CVP (caudal vein plexus), ISV (intersegmental vessel), TRIM family, angiogenesis, ftr82, zebrafish
- MeSH Terms
-
- Animals
- Biomarkers/metabolism
- Blood Circulation
- Body Patterning*/genetics
- Edema/pathology
- Gene Expression Regulation, Developmental
- Gene Knockdown Techniques
- Neovascularization, Physiologic*/genetics
- RNA, Messenger/genetics
- RNA, Messenger/metabolism
- Receptors, Notch/metabolism
- Signal Transduction
- Vascular Endothelial Growth Factor Receptor-2/metabolism
- Zebrafish/embryology*
- Zebrafish/genetics
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism*
- PubMed
- 28098794 Full text @ Int. J. Mol. Sci.
Citation
Chang, H.W., Wang, W.D., Chiu, C.C., Chen, C.H., Wang, Y.S., Chen, Z.Y., Liu, W., Tai, M.H., Wen, Z.H., Wu, C.Y. (2017) Ftr82 Is Critical for Vascular Patterning during Zebrafish Development. International Journal of Molecular Sciences. 18(1).
Abstract
Cellular components and signaling pathways are required for the proper growth of blood vessels. Here, we report for the first time that a teleost-specific gene ftr82 (finTRIM family, member 82) plays a critical role in vasculature during zebrafish development. To date, there has been no description of tripartite motif proteins (TRIM) in vascular development, and the role of ftr82 is unknown. In this study, we found that ftr82 mRNA is expressed during the development of vessels, and loss of ftr82 by morpholino (MO) knockdown impairs the growth of intersegmental vessels (ISV) and caudal vein plexus (CVP), suggesting that ftr82 plays a critical role in promoting ISV and CVP growth. We showed the specificity of ftr82 MO by analyzing ftr82 expression products and expressing ftr82 mRNA to rescue ftr82 morphants. We further showed that the knockdown of ftr82 reduced ISV cell numbers, suggesting that the growth impairment of vessels is likely due to a decrease of cell proliferation and migration, but not cell death. In addition, loss of ftr82 affects the expression of vascular markers, which is consistent with the defect of vascular growth. Finally, we showed that ftr82 likely interacts with vascular endothelial growth factor (VEGF) and Notch signaling. Together, we identify teleost-specific ftr82 as a vascular gene that plays an important role for vascular development in zebrafish.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping