小分子核醣核酸由小片段且不會轉譯成蛋白質的核醣核酸所組成，其可以藉由抑制訊息核醣核酸的轉譯作用或是促進訊息核醣核酸降解，達到調控基因表現的目的，並且其參與廣泛的生命過程，像是細胞發育、增殖、凋亡和代謝。近期的研究已釐清神經中的小分子核醣核酸在神經細胞發育和成熟的不同階段，包括神經突生長，樹突生成以及突觸形成中所扮演的角色。在許多神經退化性疾病，如阿茲海默症和帕金森氏症，皆有發現小分子核醣核酸的表現量有異常的情形。我們實驗室先前發表的文獻中發現，特定的小分子核醣核酸196a，在細胞、基因轉殖小鼠以及從患者身上取得的誘導性多功能幹細胞等亨丁頓舞蹈症模型中，皆發現此疾病有被改善的情形，暗示小分子核醣核酸196a可能在神經保護作用中扮演重要的角色。因為神經保護作用可能是透過抗氧化，抗發炎，抗細胞凋亡，細胞增生或促進神經突生長等作用，因此我們推測小分子核醣核酸196a可能會透過這些機制的其中一種，使其具有神經保護作用。在本篇論文中，我們將重點放在小分子核醣核酸196a對神經突生長的影響。在體外實驗的結果發現，小分子核醣核酸196a大量表現之後，在小鼠神經瘤母細胞中可以觀察到神經突生長促進的效果。除此之外，我們發現，與神經突生長相關的重要基因，磷酸化神經生長相關蛋白43和磷酸化細胞外訊號調節激酶1及2，在小鼠神經瘤母細胞大量表現小分子核醣核酸196a後，其蛋白質的表現量有顯著的增加。接著，在體內實驗的結果中，小分子核醣核酸196a基因轉殖小鼠的大腦皮層也顯示這兩種蛋白質的表現量比起野生型小鼠有顯著增加的情形。我們更進一步的發現，與突觸可塑性相關的蛋白質，囊泡相關膜蛋白1，其表現量在小分子核醣核酸196a基因轉殖小鼠中也有顯著性增加，並且這些基因轉殖小鼠的學習記憶能力呈現較好的趨勢。我們發現小分子核醣核
酸196a其中一個預測的目標基因，Ran結合蛋白10，為了探討其是否為小分子核醣核酸196a的目標基因，我們在體外以及體內的實驗中，大量表現小分子核醣核酸196a後發現Ran結合蛋白10的蛋白質表現量顯著下降。綜合我們的研究結果，發現小分子核醣核酸196a在神經生長上新的功能，此發現也許能提供亨丁頓舞蹈症潛在的治療策略。

SUMMARY
MicroRNAs (miRNAs) regulate gene expression by inhibiting translation or promoting mRNA degradation, and involve in a wide range of biological processes. Recent studies have clarified roles of neural miRNAs at different stages of neuronal development and maturation. One previous paper published from our laboratory indicated that a specific miRNA, miR-196a, ameliorates phenotypes of Huntington’s disease in cells, transgenic mice and patient-derived induced pluripotent stem cell models, indicating that miR-196a may play an important role in neuroprotection. We hypothesize miR-196a might have neuroprotective effects through one of these mechanisms. Here, we focused on the effects of miR-196a for neurite outgrowth. In the in vitro results, as miR-196a was overexpressed, promotion of neurite outgrowth was observed in neuroblastoma cells. Additionally, we found that the critical genes, phosphorylated GAP43 and phosphorylated ERK, related to morphology were significantly increased in neuroblastoma cells when miR-196a was overexpressed. Then, in the in vivo results, the brains of miR-196a transgenic mice also displayed higher expression of these two proteins compared to those of wild type mice. Furthermore, the expression of vesicle-associated membrane protein 1 (VAMP1) related to synaptic plasticity showed significantly increased in miR-196a transgenic mice, and these mice further have shown better trend of learning and memory ability. To investigate the target genes of miR-196a, we found that one target, RAN Binding Protein 10 (RANBP10), was decreased while miR-196a was overexpressed in vitro and in vivo. Our results identified a novel function of miR-196a in neurogenesis, and may provide a potential therapeutic strategy for neurodegenerative disease.
Key words：miR-196a、neurite outgrowth、transgenic mice

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