Abstract
Purpose :
Transmembrane protein 30A (TMEM30A) is a β-subunit of P4-ATPases, which plays important roles in folding and transporting of P4 ATPases to its cellular destination. Loss of Tmem30a leads photoreceptor degeneration in mice, however, its function in retinal vascular was not yet been elucidated. The purpose of this research was to study the function of Tmem30a gene in retina vascular development.
Methods :
We generated Tmem30a conditional knockout mice in endothelial cells using PDGFB-cre and induced global knockout mice using Cag-cre to study the function of Tmem30a gene in retina vascular development. Retina whole-mount and immunofluorescence were used to study the phenotypes of the Tmem30a conditional knockout mice. Western blotting and real-time PCR method were utilized to illustrate the underlying mechanisms.
Results :
As results, we found that when Tmem30a was removed from endothelial cell, the retina vascular development was impaired: retarded angiogenesis to the retinal peripheral zone and deep layers; decreased tip-cell number and slower endothelial cell proliferation compared to wild-type mice. Mechanically, loss of Tmem30a impaired the Vegfr2-Erk signaling pathway.
Conclusions :
Tmem30a plays critical roles in retina vascular development.
This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.