Oxidative stress retards vascular development before neural degeneration occurs in retinal degeneration rd1 mice

Abstract

To investigate the role of reactive oxygen species (ROS) in retinal development during the early postnatal stage of rd1 mice. Development of the three retinal vascular layers of C57BL/6J (WT) and C3H/HeN (rd1) mice was evaluated from 9th postnatal day (P9) to P21. Retinal ROS production was semi-quantitatively measured using dihydroethidium fluorescence. Mice were treated with intraperitoneal injections of 4-hydroxy-2,2,6,6-tetramethylpiperidin-1-oxyl (TEMPOL) at a dose of 275mg/kg body weight, and PBS as the control from P3 to P8. Rd1 mice showed retardation of retinal vascular development in the deep layer at P9. No significant difference was observed in the outer nuclear layer thickness of rd1 and WT mice. ROS production in the outer nuclear layer of rd1 mice was significantly higher than that in the outer nuclear layer of WT mice at P9, P13, and P17 (P < .05). TEMPOL facilitated the development of the deep vascular layer when compared with injection of PBS. Retardation of retinal vascular development is observed in rd1 mice; ROS is partially responsible for this finding. When using rd1 mice, we should be aware of this difference in comparison to other retinal degeneration animal models and human pathophysiological changes.