Shinichi Fukuda1, Osamu Ohneda, Tetsuro Oshika. 1. Department of Ophthalmology, Institute of Clinical Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki, 305-8575, Japan, caesar.shihtzu@gmail.com.
Abstract
PURPOSE: To investigate the role of reactive oxygen species (ROS) in retinal development during the early postnatal stage of rd1 mice. METHODS: Development of the three retinal vascular layers of C57BL/6 J (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 275 mg/kg body weight, and PBS as the control from P3 to P8. RESULTS: 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. CONCLUSIONS: 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.
PURPOSE: To investigate the role of reactive oxygen species (ROS) in retinal development during the early postnatal stage of rd1mice. METHODS: Development of the three retinal vascular layers of C57BL/6 J (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 275 mg/kg body weight, and PBS as the control from P3 to P8. RESULTS:Rd1mice 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 rd1mice 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. CONCLUSIONS:Retardation of retinal vascular development is observed in rd1mice; ROS is partially responsible for this finding. When using rd1mice, we should be aware of this difference in comparison to other retinal degeneration animal models and human pathophysiological changes.
Authors: Baerbel Rohrer; Francisco R Pinto; Kathryn E Hulse; Heather R Lohr; Li Zhang; Jonas S Almeida Journal: J Biol Chem Date: 2004-06-24 Impact factor: 5.157
Authors: B Chang; N L Hawes; M T Pardue; A M German; R E Hurd; M T Davisson; S Nusinowitz; K Rengarajan; A P Boyd; S S Sidney; M J Phillips; R E Stewart; R Chaudhury; J M Nickerson; J R Heckenlively; J H Boatright Journal: Vision Res Date: 2007-01-30 Impact factor: 1.886
Authors: Atsushi Otani; Michael Ian Dorrell; Karen Kinder; Stacey K Moreno; Steven Nusinowitz; Eyal Banin; John Heckenlively; Martin Friedlander Journal: J Clin Invest Date: 2004-09 Impact factor: 14.808
Authors: Bruce A Berkowitz; Robert H Podolsky; Ali M Berri; Kristin Dernay; Emma Graffice; Fatema Shafie-Khorassani; Robin Roberts Journal: Invest Ophthalmol Vis Sci Date: 2018-03-01 Impact factor: 4.799
Authors: Bruce A Berkowitz; Alfred S Lewin; Manas R Biswal; Bryce X Bredell; Christopher Davis; Robin Roberts Journal: Invest Ophthalmol Vis Sci Date: 2016-02 Impact factor: 4.799