Technical brief: Constant intense light exposure to lesion and initiate regeneration in normally pigmented zebrafish

Technical brief: Constant intense light exposure to lesion and initiate regeneration in normally pigmented zebrafish
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DOI:
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发表时间:
2014-07
期刊:
影响因子:
2.2
通讯作者:
Kamya Rajaram;E. Summerbell;J. G. Patton
Kamya Rajaram;E. Summerbell;J. G. Patton
中科院分区:
医学4区
文献类型:
--
作者:
Kamya Rajaram;E. Summerbell;J. G. Patton

文献摘要

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斑马鱼能够对受损的视网膜进行稳健和自发的再生。成年白化病斑马鱼持续的强光照射可以特异性地引起视杆细胞和视锥细胞的凋亡,是研究光感受器再生分子机制的理想模型。然而,这种模式只适用于病变斑马鱼的nonpigmented白化病的遗传背景,这排除了使用大量的转基因报告线,广泛用于研究再生。在这里,我们探讨了持续强光照射在正常色素的斑马鱼视网膜中引起感光细胞凋亡和刺激再生的有效性。我们发现,持续的强光照射会导致色素斑马鱼背中央视网膜的感光细胞广泛受损。光感受器丧失触发Müller胶质细胞的去分化和增殖以及祖细胞增殖。我们还证明了再生反应的时间轴在白化病和色素视网膜之间是相当的。
Zebrafish are capable of robust and spontaneous regeneration of injured retina. Constant intense light exposure to adult albino zebrafish specifically causes apoptosis of rod and cone photoreceptor cells and is an excellent model to study the molecular mechanisms underlying photoreceptor regeneration. However, this paradigm has only been applied to lesion zebrafish of the nonpigmented albino genetic background, which precludes the use of numerous transgenic reporter lines that are widely used to study regeneration. Here, we explored the effectiveness of constant intense light exposure in causing photoreceptor apoptosis and stimulating regeneration in normally pigmented zebrafish retinas. We show that constant intense light exposure causes widespread photoreceptor damage in the dorsal-central retinas of pigmented zebrafish. Photoreceptor loss triggers dedifferentiation and proliferation of Müller glia as well as progenitor cell proliferation. We also demonstrate that the timeline of regeneration response is comparable between the albino and the pigmented retinas.