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MicroRNA Expression Profile and Functional Analysis Reveal that miR-206 is a Critical Novel Gene for the Expression of BDNF Induced by Ketamine

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Abstract

Depression is a major social and health concern, and ketamine exerts a quick, remarkable and persistent anti-depressive effect. microRNAs (miRNAs) show remarkable potential in the treatment of clinical depression. Here, we determined the expression profile of miRNAs in the hippocampus of rats treated with ketamine (15 mg/kg). The results suggest that multiple miRNAs were aberrantly expressed in rat hippocampus after ketamine injection (18 miRNAs were significantly reduced, while 22 miRNAs were significantly increased). Among them, miR-206 was down-regulated in ketamine-treated rats. In both cultured neuronal cells in vitro and hippocampus in vivo, we identified that the brain-derived neurotrophic factor (BDNF) was a direct target gene of miR-206. Via this target gene, miR-206 strongly modulated the expression of BDNF. Moreover, overexpression of miR-206 significantly attenuated ketamine-induced up-regulation of BDNF. The results indicated that miRNA-206 was involved in novel therapeutic targets for the anti-depressive effect of ketamine.

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Acknowledgments

This project was supported by the Projects of the National Natural Science Foundation of China (Grant No. 8127147) and International Cooperation, Department of Science & Technology of Sichuan Province (Grant No. 2011HH0031) to X. Wang. The authors acknowledge Yong Pu and Haidong Wu Ph.D. from Saier Biotechnology Inc. for their laboratory support and Tingjing Gong Ph.D. from Tianjing Kangchen Biotechnology Inc. for his support and encouragement with this research project.

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The authors have declared no conflict of interest in this matter.

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Correspondence to Xiaobin Wang.

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Yang, X., Yang, Q., Wang, X. et al. MicroRNA Expression Profile and Functional Analysis Reveal that miR-206 is a Critical Novel Gene for the Expression of BDNF Induced by Ketamine. Neuromol Med 16, 594–605 (2014). https://doi.org/10.1007/s12017-014-8312-z

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  • DOI: https://doi.org/10.1007/s12017-014-8312-z

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