Zheng Jiaolin, Yi Dan, Shi Xiaodong, Shi Huaizhang
Department of Neruology, The second hospital of Harbin Medical University, Harbin, Heilong Jiang, 150086, China.
Department of Pharmacology, Rush University Medical Center, Chicago, IL, 60607, USA.
Cell Prolif. 2017 Aug;50(4). doi: 10.1111/cpr.12347. Epub 2017 May 2.
Neural stem cells (NSCs) are self-renewing, undifferentiated and multipotent precursors that can generate neuronal and glial lineages. MicroRNAs (miRNAs) are small non-coding RNAs that act crucial roles in cell proliferation, differentiation and migration. However, the role of miR-1297 in the development of NSCs is still unknown.
Primary NSCs were isolated from rat's embryos. The expression of miR-1297 and Hes1 were measured by qRT-PCR. Western blot was performed to detect the protein expression of Hes1, β-tubulin-III and GFAP.
We showed that miR-1297 expression was upregulated during NSC differentiation, while the expression of Hes1 was decreased during NSC differentiation. Elevated expression of miR-1297 promoted the NSCs viability and increased the formation of NSCs to neurospheres. Ecoptic expression of miR-1297 promoted β-tubulin-III expression in the NSCs. Overexpression of miR-1297 decreased GFAP expression in the NSCs. Furthermore, we demonstrated that miR-1297 regulated NSCs viability and differentiation by directly targeting Hes1. Overexpression of miR-1297 suppressed Hes1 expression in the NSCs.
These results suggested that miR-1297 played an important role in NSCs viability and differentiation through inhibiting Hes1 expression.
神经干细胞(NSCs)是自我更新、未分化且具有多能性的前体细胞,能够产生神经元和神经胶质谱系细胞。微小RNA(miRNAs)是一类小的非编码RNA,在细胞增殖、分化和迁移中发挥关键作用。然而,miR-1297在神经干细胞发育中的作用仍不清楚。
从大鼠胚胎中分离出原代神经干细胞。通过qRT-PCR检测miR-1297和Hes1的表达。进行蛋白质免疫印迹法检测Hes1、β-微管蛋白III和胶质纤维酸性蛋白(GFAP)的蛋白表达。
我们发现,在神经干细胞分化过程中miR-1297表达上调,而Hes1表达下降。miR-1297表达升高促进了神经干细胞的活力,并增加了神经干细胞形成神经球的数量。miR-1297异位表达促进了神经干细胞中β-微管蛋白III的表达。miR-1297过表达降低了神经干细胞中GFAP的表达。此外,我们证明miR-1297通过直接靶向Hes1来调节神经干细胞的活力和分化。miR-1297过表达抑制了神经干细胞中Hes1的表达。
这些结果表明,miR-1297通过抑制Hes1表达在神经干细胞的活力和分化中发挥重要作用。