Tso M O, Zhang C, Abler A S, Chang C J, Wong F, Chang G Q, Lam T T
Department of Ophthalmology and Visual Sciences, UIC Eye Center, University of Illinois at Chicago College of Medicine 60612.
Invest Ophthalmol Vis Sci. 1994 May;35(6):2693-9.
To determine the pathogenetic mechanism of photoreceptor cell degeneration in the inherited retinal dystrophy in Royal College of Surgeons (RCS) rats.
The dystrophic retinas of the pink-eyed RCS (RCS-rdy-p) rats were examined for DNA fragmentation by agarose gel electrophoresis of retinal DNA and by TdT-mediated biotin-dUDP nick-end labeling (TUNEL) in paraffin sections. Rats ranging in age from 3 to 60 days were examined.
Agarose gel electrophoresis of retinal DNA isolated from animals 25, 30, 35, and 40 days old showed a ladder pattern of degradation with bands corresponding to multiples of 180 to 200 base pair subunits. TUNEL study showed increasing labeling of photoreceptor cells with progression of the retinal dystrophy of the RCS rats.
Apoptosis is the dominant mechanism of photoreceptor degeneration in the RCS rat, which has a genetic defect in the phagocytic activity of retinal pigment epithelium. The onset of the degeneration appeared to vary between rod cells in the different regions of the eye.
确定皇家外科学院(RCS)大鼠遗传性视网膜营养不良中光感受器细胞变性的发病机制。
通过对视网膜DNA进行琼脂糖凝胶电泳以及对石蜡切片进行TdT介导的生物素-dUDP缺口末端标记(TUNEL),检查粉红色眼睛的RCS(RCS-rdy-p)大鼠的营养不良视网膜。检查了年龄在3至60天的大鼠。
从25、30、35和40日龄动物分离的视网膜DNA的琼脂糖凝胶电泳显示出降解的梯状模式,条带对应于180至200个碱基对亚基的倍数。TUNEL研究表明,随着RCS大鼠视网膜营养不良的进展,光感受器细胞的标记增加。
细胞凋亡是RCS大鼠光感受器变性的主要机制,RCS大鼠在视网膜色素上皮的吞噬活性方面存在遗传缺陷。变性的起始似乎在眼睛不同区域的视杆细胞之间有所不同。