Purchase this article with an account.
Jing Lu, Lin Lu, Yan Luo; Claudin-3 regulates hyaloid vessel formation and retinal development in zebrafish. Invest. Ophthalmol. Vis. Sci. 2018;59(9):5492.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Claudin-3 (cldn3), a tight junction integral protein, was involved in the genesis of blood-brain barrier. However, the role of cldn3 in vascular formation elsewhere remains unclear. We investigated the role of cldn3 in hyaloid vessel formation and its relation to retinal development in zebrafish.
Cldn3 protein expression in the flk:GFP transgenic zebrafish was knocked down using splice Morpholino (MO). The morphology of hyaloid vessels and retina was observed, and the permeability of retinal vasculatures was examined post microinjection. Proliferation and apoptosis of the endothelial and retinal cells were detected using BrdU and TUNEL. Rescue experiments were performed to further support the specificity of cldn3 MO-induced phenotype.
Cldn3 protein was expressed in the lens, retinal cells, optical nerves, and endothelial cells of hyaloid vessels. MO-induced knockdown of cldn3 in zebrafish resulted in density reduction of hyaloid vessels. Increased vascular leakage of retinal vessels were observed. Delayed retinal differentiation and thinned neuroretina were also detected. The endothelial and retinal cells showed reduced proliferation and increased apoptosis at 36 hours post fertilization. Coinjection of the RNA encoding cldn3 together with the splice MO rescued the abnormal phenotype.
Together, our data suggest that cldn3 knockdown results in abnormal development of the retina and hyaloid vessels in zebrafish.
This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.
This PDF is available to Subscribers Only