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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 >A distinct effect of transient and sustained upregulation of cellular factor XIII in the goldfish retina and optic nerve on optic nerve regeneration
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A distinct effect of transient and sustained upregulation of cellular factor XIII in the goldfish retina and optic nerve on optic nerve regeneration

机译：金鱼视网膜和视神经中细胞因子XIII的瞬时和持续上调对视神经再生的明显影响

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Unlike in mammals, fish retinal ganglion cells (RGCs) have a capacity to repair their axons even after optic nerve transection. In our previous study, we isolated a tissue type transglutaminase (TG) from axotomized goldfish retina. The levels of retinal TG (TG R) mRNA increased in RGCs 1-6 weeks after nerve injury to promote optic nerve regeneration both in vitro and in vivo. In the present study, we screened other types of TG using specific FITC-labeled substrate peptides to elucidate the implications for optic nerve regeneration. This screening showed that the activity of only cellular coagulation factor XIII (cFXIII) was increased in goldfish optic nerves just after nerve injury. We therefore cloned a full-length cDNA clone of FXIII A subunit (FXIII-A) and studied temporal changes of FXIII-A expression in goldfish optic nerve and retina during regeneration. FXIII-A mRNA was initially detected at the crush site of the optic nerve 1 h after injury; it was further observed in the optic nerve and achieved sustained long-term expression (1-40 days after nerve injury). The cells producing FXIII-A were astrocytes/microglial cells in the optic nerve. By contrast, the expression of FXIII-A mRNA and protein was upregulated in RGCs for a shorter time (3-10 days after nerve injury). Overexpression of FXIII-A in RGCs achieved by lipofection induced significant neurite outgrowth from unprimed retina, but not from primed retina with pretreatment of nerve injury. Addition of extracts of optic nerves with injury induced significant neurite outgrowth from primed retina, but not from unprimed retina without pretreatment of nerve injury. The transient increase of cFXIII in RGCs promotes neurite sprouting from injured RGCs, whereas the sustained increase of cFXIII in optic nerves facilitates neurite elongation from regrowing axons.
机译：与哺乳动物不同，鱼的视网膜神经节细胞（RGC）即使在视神经横断后也具有修复其轴突的能力。在我们以前的研究中，我们从切除了轴突的金鱼的视网膜中分离了一种组织型转谷氨酰胺酶（TG）。神经损伤后1-6周，RGC中视网膜TG（TG R）mRNA水平增加，从而促进了体内外的视神经再生。在本研究中，我们使用特定的FITC标记的底物肽筛选了其他类型的TG，以阐明对视神经再生的影响。此筛选显示，仅在神经损伤后，金鱼视神经中仅细胞凝血因子XIII（cFXIII）的活性增加。因此，我们克隆了FXIII A亚基（FXIII-A）的全长cDNA克隆，并研究了再生期间金鱼视神经和视网膜中FXIII-A表达的时间变化。受伤后1小时，在视神经的压迫部位初步检测到了FXIII-A mRNA。在视神经中进一步观察到它，并实现了持续的长期表达（神经损伤后1-40天）。产生FXIII-A的细胞是视神经中的星形胶质细胞/小胶质细胞。相反，在较短的时间（神经损伤后3-10天）中，RGC中的FXIII-A mRNA和蛋白的表达上调。通过脂转染实现的RGC中FXIII-A的过表达诱导未刺激视网膜产生明显的神经突生长，但预处理神经损伤后未引发视网膜。在未进行神经损伤的预处理的情况下，添加视神经损伤的提取物可引起明显的神经突生长，而未引发的视网膜则无此现象。 RGC中cFXIII的短暂增加促进了受损RGC中的神经突萌发，而视神经中cFXIII的持续增加则促进了轴突生长引起的神经突伸长。

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