The effect of oxygen on retinal degeneration in wild-type and hsp70.1 knockout neonatal retinal degeneration mice.

Choi,  M Y; Yu,  Y S; Kim,  S K; Kim,  Y J; Seo,  J S

doi:2001.15.1.1

Korean J Ophthalmol > Volume 15(1); 2001 > Article

Research Support, Non-U.S. Gov't

Korean Journal of Ophthalmology 2001;15(1):1-7.
DOI: https://doi.org/10.3341/kjo.2001.15.1.1 Published online June 30, 2001.

The effect of oxygen on retinal degeneration in wild-type and hsp70.1 knockout neonatal retinal degeneration mice.

M Y Choi, Y S Yu, S K Kim, Y J Kim, J S Seo

Department of Ophthalmology, College of Medicine, Chungbuk National University & Chungbuk National University Medical Research Institute, Cheongju, Korea.

Abstract

The present study examined the effect of oxygen on photoreceptor degeneration in the retina of heat shock protein 70.1 (hsp70.1) knockout type and wild-type retinal degeneration (rd) mice. All the neonatal rd mice were exposed to hyperoixa for 5 days after birth, and then were returned to room air before being sacrificed. At the postnatal 10, 14, 18, and 21 days, the ratio of outer nuclear layer (ONL) thickness to total retinal thickness was compared between hsp70.1 knockout type and wild type. The retina was also examined for DNA fragmentation by TdT-mediated biotin-dUTP nick-end labeling (TUNEL). In hsp70.1 knockout type, the ratio of ONL to total retinal thickness was higher than that in the wild type at each time. There was the remarkable difference in the number and distribution of TUNEL-positive cells between hsp70.1 knockout type and wild type rd mice. In conclusion, an oxygen-induced modulation of the rate of photoreceptor degeneration was more marked in the hsp70.1 knockout type than wild type rd mice.