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Gao, Fang; Zhang, Yu-Fei; Zhang, Zheng-Ping; Fu, Luo-An; Cao, Xiu-Li; Zhang, Yi-Zhe; Guo, Chen-Jun; Yan, Xian-Chun; Yang, Qin-Chuan; Hu, Yi-Yang; Zhao, Xiang-Hui; Wang, Ya-Zhou; Wu, Sheng-Xi; Ju, Gong; Zheng, Min-Hua; Han, Hua
Stem cell reports, 04/2017, Volume: 8, Issue: 4Journal Article
Notch signaling is critically involved in neural development, but the downstream effectors remain incompletely understood. In this study, we cultured neurospheres from Nestin-Cre-mediated conditional Rbp-j knockout (Rbp-j cKO) and control embryos and compared their miRNA expression profiles using microarray. Among differentially expressed miRNAs, miR-342-5p showed upregulated expression as Notch signaling was genetically or pharmaceutically interrupted. Consistently, the promoter of the miR-342-5p host gene, the Ena-vasodilator stimulated phosphoprotein-like (Evl), was negatively regulated by Notch signaling, probably through HES5. Transfection of miR-342-5p promoted the differentiation of neural stem cells (NSCs) into intermediate neural progenitors (INPs) in vitro and reduced the stemness of NSCs in vivo. Furthermore, miR-342-5p inhibited the differentiation of neural stem/intermediate progenitor cells into astrocytes, likely mediated by targeting GFAP directly. Our results indicated that miR-342-5p could function as a downstream effector of Notch signaling to regulate the differentiation of NSCs into INPs and astrocytes commitment. Display omitted •miR-342-5p acts as a downstream effector of canonical Notch signaling•Notch signal inhibits miR-342-5p expression by regulating its host gene Evl•miR-342-5p promotes the transition of NSCs into INPs•Astrocyte commitment was suppressed by miR-342-5p targeting GFAP In this article, Han and colleagues show that miR-342-5p acts as a downstream effector of Notch signaling in the mouse CNS. Notch signal inhibits miR-342-5p expression by regulating its host gene Evl. And with attenuated Notch signal in NSCs, miR-342-5p is upregulated to promote NSCs transition into INPs, and to inhibit astrocyte commitment by targeting GFAP.
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