PUBLICATION
Knockdown of zebrafish blood vessel epicardial substance results in incomplete retinal lamination
- Authors
- Wu, Y.C., Chen, R.F., Liu, C.Y., Hu, F.R., Huang, C.J., Wang, I.J.
- ID
- ZDB-PUB-140513-130
- Date
- 2014
- Source
- TheScientificWorldJournal 2014: 803718 (Journal)
- Registered Authors
- Huang, Chang-Jen
- Keywords
- none
- MeSH Terms
-
- Animals
- Animals, Genetically Modified
- Base Sequence
- Cell Polarity
- DNA Primers
- Retina/cytology*
- Retinal Vessels/metabolism*
- Zebrafish*
- PubMed
- 24741362 Full text @ ScientificWorldJournal
Citation
Wu, Y.C., Chen, R.F., Liu, C.Y., Hu, F.R., Huang, C.J., Wang, I.J. (2014) Knockdown of zebrafish blood vessel epicardial substance results in incomplete retinal lamination. TheScientificWorldJournal. 2014:803718.
Abstract
Cell polarity during eye development determines the normal retinal lamination and differentiation of photoreceptor cells in the retina. In vertebrates, blood vessel epicardial substance (Bves) is known to play an important role in the formation and maintenance of the tight junctions essential for epithelial cell polarity. In the current study, we generated a transgenic zebrafish Bves (zbves) promoter-EGFP zebrafish line to investigate the expression pattern of Bves in the retina and to study the role of zbves in retinal lamination. Immunostaining with different specific antibodies from retinal cells and transmission electron microscopy were used to identify the morphological defects in normal and Bves knockdown zebrafish. In normal zebrafish, Bves is located at the apical junctions of embryonic retinal neuroepithelia during retinogenesis; later, it is strongly expressed around inner plexiform layer (IPL) and retinal pigment epithelium (RPE). In contrast, a loss of normal retinal lamination and cellular polarity was found with undifferentiated photoreceptor cells in Bves knockdown zebrafish. Herein, our results indicated that disruption of Bves will result in a loss of normal retinal lamination.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping