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延缓rd1小鼠视网膜脱离后光感受器的退化

Retardation of photoreceptor degeneration in the detached retina of rd1 mouse.

作者信息

Kaneko Hiroki, Nishiguchi Koji M, Nakamura Makoto, Kachi Shu, Terasaki Hiroko

机构信息

Department of Ophthalmology, Nagoya University Graduate School of Medicine, Nagoya, Japan.

出版信息

Invest Ophthalmol Vis Sci. 2008 Feb;49(2):781-7. doi: 10.1167/iovs.07-0715.

Abstract

PURPOSE

To study the neuroprotective effect of experimental retinal detachment (RD) on photoreceptor degeneration in rd1 mice.

METHODS

RD was produced in the eyes of rd1 mice at postnatal day (P) 9. These eyes were collected and compared to controls without RD. The effects of RD on retinal degeneration were evaluated by histochemical staining of nuclei in the outer nuclear layer (ONL), rod and cone photoreceptors, and retinal vessels at P30 in retinal sections and flatmounts. Apoptotic photoreceptors were detected by TdT-mediated dUTP nick-end labeling (TUNEL) at P15. Mice with or without RD were also reared in darkness and evaluated immunohistochemically at P30.

RESULTS

The numbers of rhodopsin-positive (rod), peanut agglutinin-positive (cone), and diamino-2-phenyl-indol-stained (rod-plus-cone) cells in the ONL were increased by 2.0-fold, 1.3-fold, and 1.2-fold, respectively, in the rd1 eyes with RD compared to those without RD at P30. In the detached retina, the cone photoreceptor inner/outer segment structures and the deep retinal vessels surrounding the inner nuclear layer and the ONL, but not the ganglion cell layer, were preserved. At P15, TUNEL-positive cell numbers in the ONL were significantly reduced in the eyes with RD. Light exposure had no effect on photoreceptor degeneration in the eyes with or without RD.

CONCLUSIONS

RD mediates the preservation of cone and rod photoreceptors in the ONL and surrounding vascular structures by reducing the rate of apoptosis of photoreceptors in rd1 mice. Light deprivation does not appear to be one of the mechanisms of photoreceptor protection in the detached retinas in these mice.

摘要

目的

研究实验性视网膜脱离(RD)对rd1小鼠光感受器退变的神经保护作用。

方法

在出生后第9天(P9)对rd1小鼠的眼睛造成视网膜脱离。收集这些眼睛并与未发生视网膜脱离的对照组进行比较。通过对视网膜切片和平铺标本中P30时外核层(ONL)、视杆和视锥光感受器以及视网膜血管中的细胞核进行组织化学染色,评估视网膜脱离对视网膜退变的影响。在P15时通过末端脱氧核苷酸转移酶介导的dUTP缺口末端标记法(TUNEL)检测凋亡的光感受器。有或没有视网膜脱离的小鼠也在黑暗中饲养,并在P30时进行免疫组织化学评估。

结果

在P30时,与未发生视网膜脱离的rd1小鼠眼睛相比,发生视网膜脱离的rd1小鼠眼睛中,ONL中视紫红质阳性(视杆)、花生凝集素阳性(视锥)和二氨基-2-苯基吲哚染色(视杆加视锥)细胞的数量分别增加了2.0倍、1.3倍和1.2倍。在脱离的视网膜中,视锥光感受器的内/外段结构以及围绕内核层和ONL的深层视网膜血管得以保留,但神经节细胞层未保留。在P15时,发生视网膜脱离的眼睛中ONL中TUNEL阳性细胞数量显著减少。光照对有或没有视网膜脱离的眼睛中的光感受器退变没有影响。

结论

视网膜脱离通过降低rd1小鼠光感受器的凋亡率,介导了ONL中视锥和视杆光感受器以及周围血管结构的保留。在这些小鼠中,光剥夺似乎不是脱离视网膜中光感受器保护的机制之一。

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