A novel model of retinal ablation demonstrates that the extent of rod cell death regulates the origin of the regenerated zebrafish rod photoreceptors.
A novel model of retinal ablation demonstrates that the extent of rod cell death regulates the origin of the regenerated zebrafish rod photoreceptors.
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DOI：
10.1002/cne.22243
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发表时间：
2010-03-15
期刊：
影响因子：
--
通讯作者：
Hyde DR
中科院分区：
文献类型：
--
作者：
Montgomery JE;Parsons MJ;Hyde DR
成年斑马鱼视网膜继续从不频繁的müller神经胶质细胞分裂产生杆状感受器，产生迁移到外部核层的神经元祖细胞，并成为杆的杆前体细胞，这些细胞有助于区分杆状细胞模型。从杆前体细胞中，虽然任何其他残留神经元的丧失激活müller神经胶质增殖，从而产生多能神经元祖细胞，这些神经元祖细胞可以在视网膜中产生任何其他神经元细胞类型。仅在杆上融合到EGFP（NTR-EGFP）。对比度的神经祖细胞的簇，仅在TG上烧毁一部分杆（ZOP：NFSB-EGFP）NT20视网膜，导致了杆前体，但不建议使用MüllerGlial，但我们提出了两个不同的标准。死亡将诱发Müller神经胶质的再生反应，而不是从ONL中的固定杆前体细胞。而不是慢性，刺激Müller神经胶质的再生。
The adult zebrafish retina continuously produces rod photoreceptors from infrequent Müller glial cell division, yielding neuronal progenitor cells that migrate to the outer nuclear layer and become rod precursor cells that are committed to differentiate into rods. Retinal damage models suggested that rod cell death induces regeneration from rod precursor cells, whereas loss of any other retinal neurons activates Müller glia proliferation to produce pluripotent neuronal progenitors that can generate any other neuronal cell type in the retina. We tested this hypothesis by creating two transgenic lines that expressed the E. coli nitroreductase enzyme fused to EGFP (NTR-EGFP) in only rods. Treating transgenic adults with metronidazole resulted in two rod cell death models. First, killing all rods throughout the Tg(zop:nfsB-EGFP)nt19 retina induced robust Müller glial proliferation, which yielded clusters of neuronal progenitor cells. In contrast, ablating only a subset of rods across the Tg(zop:nfsB-EGFP)nt20 retina led to rod precursor, but not Müller glial, cell proliferation. We propose that two different criteria determine whether rod cell death will induce a regenerative response from the Müller glia rather than from the resident rod precursor cells in the ONL. First, there must be a large amount of rod cell death to initiate Müller glia proliferation. Second, the rod cell death must be acute, rather than chronic, to stimulate regeneration from the Müller glia. This suggests that the zebrafish retina possesses mechanisms to quantify the amount and timing of rod cell death.
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影响因子：
2.7
作者：
Davison, Jon M.;Akitake, Courtney M.;Parsons, Michael J.
通讯作者：
Parsons, Michael J.
影响因子：
16.2
作者：
TREVARROW, B;MARKS, DL;KIMMEL, CB
通讯作者：
KIMMEL, CB
影响因子：
5.3
作者：
Bernardos, Rebecca L.;Barthel, Linda K.;Raymond, Pamela A.
通讯作者：
Raymond, Pamela A.
DOI：
10.1016/0006-291x(86)90744-8
发表时间：
1986-11-14
影响因子：
3.1
作者：
ROBERTS, JJ;FRIEDLOS, F;KNOX, RJ
通讯作者：
KNOX, RJ
影响因子：
2.5
作者：
Curado, Silvia;Anderson, Ryan M.;Stainier, Didier Y. R.
通讯作者：
Stainier, Didier Y. R.