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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Involvement of retinoic acid signaling in goldfish optic nerve regeneration.
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Involvement of retinoic acid signaling in goldfish optic nerve regeneration.

机译：视黄酸信号参与金鱼视神经再生。

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Recently, we identified a retina-specific retinol-binding protein, purpurin, as a trigger molecule in the early stage of goldfish optic nerve regeneration. Purpurin protein was secreted by photoreceptors to injured ganglion cells, at 2-5 days after optic nerve injury. Purpurin bound to retinol induced neurite outgrowth in retinal explant cultures and retinoic acid (RA) had a comparable effect on neurite outgrowth. These results indicate that purpurin acts as a retinol transporter and facilitates conversion of retinol to RA. Intracellularly, RA is transported into the nucleus with cellular retinoic acid-binding protein IIb (CRABPIIb) and binds with retinoic acid receptor alpha (RARalpha) as a transcriptional regulator of target genes. Here, we investigated the RA signaling through RA synthesis to RARalpha in the goldfish retina during optic nerve regeneration by RT-PCR. Retinaldehyde dehydrogenase 2 (RALDH2; an RA synthetic enzyme) mRNA was increased by 2.7-fold in the retina at 7-10 days and then gradually decreased until 40 days after nerve injury. In contrast, cytochrome P450 26a1 (CYP26a1; an RA degradative enzyme) mRNA was decreased to less than half in the retina at 5-20 days and then gradually returned to the control level by 40 days after nerve injury. CRABPIIb mRNA was increased by 1.5-fold in the retina at 10 days after axotomy, RARalphaa mRNA was increased by 1.8-fold in the retina at 10 days after axotomy. The cellular changes in the RA signaling molecules after optic nerve injury were almost all located in the ganglion cells, as evaluated by in situ hybridization. The present data described for the first time that RA signaling through RALDH2 and CRABPIIb to RARalpha was serially upregulated in the ganglion cells at 7-10 days just after the purpurin induction. Therefore, we conclude that the triggering action of purpurin on optic nerve regeneration is mediated by RA signaling pathway.
机译：最近，我们确定了视网膜特异性视黄醇结合蛋白，紫嘌呤，作为金鱼视神经再生早期的触发分子。视神经损伤后2-5天，感光细胞将紫癜蛋白分泌到受损的神经节细胞中。在视网膜外植体培养物中，紫癜素与视黄醇诱导的神经突增生结合，而视黄酸（RA）对神经突增生具有类似的作用。这些结果表明紫嘌呤起视黄醇转运蛋白的作用，并促进视黄醇向RA的转化。在细胞内，RA与细胞视黄酸结合蛋白IIb（CRABPIIb）一起转运到细胞核中，并与视黄酸受体α（RARalpha）结合，成为靶基因的转录调节因子。在这里，我们通过RT-PCR研究了视神经再生过程中金鱼视网膜中RA合成到RARalpha的RA信号。视黄醛脱氢酶2（RALDH2;一种RA合成酶）mRNA在7-10天时视网膜中增加了2.7倍，然后逐渐下降，直到神经损伤后40天。相比之下，细胞色素P450 26a1（CYP26a1; RA降解酶）mRNA在5-20天时降至视网膜的一半以下，然后在神经损伤后40天逐渐恢复至对照水平。轴切术后第10天，视网膜中CRABPIIb mRNA增加1.5倍，轴切术后第10天，RARalphaa mRNA在视网膜中增加1.8倍。通过原位杂交评估，视神经损伤后RA信号分子中的细胞变化几乎全部位于神经节细胞中。本数据首次描述了在紫嘌呤诱导后7-10天，神经节细胞中通过RALDH2和CRABPIIb向RARalpha传递的RA信号被连续上调。因此，我们得出结论，紫癜对视神经再生的触发作用是由RA信号通路介导的。

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