| Literature DB >> 31296962 |
Jing Qiao1, Jinping Zhao1, Shujuan Chang1, Qiaoyi Sun1, Nana Liu1, Jianfeng Dong1, Yafang Chen1, Dandan Yang1, Dan Ye1, Xiaoqin Liu1, Yangyang Yu1, Wen Chen1, Songcheng Zhu1, Guiying Wang1, Wenwen Jia1, Jiajie Xi2, Jiuhong Kang3.
Abstract
Aging-related cognitive ability impairments are one of the main threats to public health, and impaired hippocampal neurogenesis is a major cause of cognitive decline during aging. However, the regulation of adult neurogenesis in the hippocampus requires further study. Here, we investigated the role of microRNA-153 (miR-153), a highly conserved microRNA in mice and humans, in adult neurogenesis. During the passaging of neural stem cells (NSCs) in vitro, endogenous miR-153 expression was downregulated, with a decrease in neuronal differentiation ability. In addition, miR-153 overexpression increased the neurogenesis of NSCs. Further studies showed that miR-153 regulated neurogenesis by precisely targeting the Notch signaling pathway through inhibition of Jagged1 and Hey2 translation. In vivo analysis demonstrated that miR-153 expression was decreased in the hippocampi of aged mice with impaired cognitive ability, and that miR-153 overexpression in the hippocampus promoted neurogenesis and markedly increased the cognitive abilities of the aged mice. Overall, our findings revealed that miR-153 affected neurogenesis by regulating the Notch signaling pathway and elucidated the function of miR-153 in aging-related, hippocampus-dependent cognitive ability impairments, and neurodegenerative diseases.Entities:
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Year: 2019 PMID： 31296962 PMCID： PMC7206122 DOI： 10.1038/s41418-019-0388-4
Source DB: PubMed Journal: Cell Death Differ ISSN： 1350-9047 Impact factor: 15.828