Prokineticin 2 Expression Is Associated with Neural Repair of Injured Adult Zebrafish Telencephalon
Prokineticin 2 Expression Is Associated with Neural Repair of Injured Adult Zebrafish Telencephalon
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DOI：
10.1089/neu.2009.0972
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发表时间：
2010-05-01
影响因子：
4.2
通讯作者：
Soussi-Yanicostas, Nadia
中科院分区：
文献类型：
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作者：
Ayari, Besma;El Hachimi, Khalid H.;Soussi-Yanicostas, Nadia
前动力蛋白2（Prokineticin 2，PROK 2）是一种分泌性蛋白，在成年哺乳动物中调节包括嗅球神经发生在内的多种生物过程。然而，其在这一过程中的确切作用尚未完全清楚。由于众所周知，成年硬骨鱼，包括斑马鱼，在几个脑区显示出强烈的增殖活性，我们利用这一特点来分析PROK2转录本在成年斑马鱼脑和损伤诱导的端脑（TC）再生过程中的分布。首先，我们表征了斑马鱼PROK2基因，并表明其转录发生在以前在成年斑马鱼大脑中鉴定的几乎所有增殖区域。此外，在TC中，PROK2的转录主要限于神经元。接下来，使用一种新的成年斑马鱼TC损伤模型，我们观察到TC损伤诱导损伤半球内邻近和远侧损伤部位的细胞增殖急剧增加。此外，我们的数据有力地表明，细胞增殖之后是新产生的神经元向损伤部位的迁移。此外，我们观察到PROK2转录本的短暂过表达，在损伤后的第一天在病变周围的细胞中检测到，并且几天后，在从TC的皮质区域向损伤部位延伸的宽细胞行中检测到。当再生过程接近完成时，不再检测到PROK2过表达，表明异位PROK2转录抑制神经元再生。总之，我们的研究结果表明，在成年斑马鱼脑中，PROK 2可能在组成性和损伤诱导的神经发生中发挥作用。
Prokineticin 2 (PROK2) is a secreted protein that regulates diverse biological processes including olfactory bulb neurogenesis in adult mammals. However, its precise role in this process is as yet not fully understood. Because it is well known that adult teleost fish, including zebrafish, display an intense proliferative activity in several brain regions, we took advantage of this feature to analyze the distribution of PROK2 transcripts in the adult zebrafish brain and during injury-induced telencephalon (TC) regeneration. First, we characterized the zebrafish PROK2 gene and showed that its transcription takes place in almost all proliferating areas previously identified in adult zebrafish brain. Moreover, in TC, PROK2 transcription was mainly restricted to neurons. Next, using a novel model of TC injury in adult zebrafish, we observed that TC lesion induced a dramatic increase in cell proliferation within the injured hemisphere in regions located both adjacent and distal to injury sites. Moreover, our data strongly suggest that cell proliferation was followed by the migration of newly generated neurons toward injury sites. In addition, we observed a transient over-expression of PROK2 transcripts, which was detected in cells surrounding the lesion during the very first days post injury, and, a few days later, in broad cell rows extending from cortical regions of the TC toward injury sites. PROK2 over-expression was no longer detected when the regeneration process was close to completion, showing that ectopic PROK2 transcription paralleled neuronal regeneration. Taken together, our results suggest that in adult zebrafish brain, PROK2 may play a role in both constitutive and injury-induced neurogenesis.