The potential regulatory mechanisms of MIR-196a in huntington's disease through bioinformatic analyses

Mu Hui Fu, Chia Ling Li, Hsiu Lien Lin, Shaw Jeng Tsai, Yen Yu Lai, Yu Fan Chang, Pei Hsun Cheng, Chuan Mu Chen, Shang Hsun Yang

研究成果: Article同行評審

35 引文 斯高帕斯(Scopus)


High throughput screening is a powerful tool to identify the potential candidate molecules involved during disease progression. However, analysis of complicated data is one of the most challenging steps on the way to obtaining useful results from this approach. Previously, we showed that a specific miRNA, miR-196a, could ameliorate the pathological phenotypes of Huntington's disease (HD) in different models, and performed high throughput screening by using the striatum of transgenic mice. In this study, we further tried to identify the potential regulatory mechanisms using different bioinformatic tools, including Database for Annotation, Visualization and Integrated Discovery (DAVID), Molecular Signatures Database (MSigDB), TargetScan and MetaCore. The results showed that miR-196a dominantly altered "ABC transporters", "RIG-I-like receptor signaling pathway", immune system", "adaptive immune system","tissue remodeling and wound repair" and "cytoskeleton remodeling". In addition, miR-196a also changed the expression of several well-defined pathways of HD, such as apoptosis and cell adhesion. Since these analyses showed the regulatory pathways are highly related to the modification of the cytoskeleton, we further confirmed that miR-196a could enhance the neurite outgrowth in neuroblastoma cells, suggesting miR-196a might provide beneficial functions through the alteration of cytoskeleton structures. Since impairment of the cytoskeleton has been reported in several neuronal diseases, this study will provide not only the potential working mechanisms of miR-196a but also insights for therapeutic strategies for use with different neuronal diseases.

期刊PloS one
出版狀態Published - 2015 9月 16

All Science Journal Classification (ASJC) codes

  • 多學科


深入研究「The potential regulatory mechanisms of MIR-196a in huntington's disease through bioinformatic analyses」主題。共同形成了獨特的指紋。