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G蛋白偶联受体Smo正向调节成年神经干细胞的增殖和迁移

[G-protein coupled receptor Smo positively regulates proliferation and migration of adult neural stem cells ].

作者信息

Qiu X, Chen H, Feng D, Dong W

机构信息

Experiment Teaching and Administration Center, Southern Medical University, Guangzhou 510515, China.

Department of Neurosurgery, Third Affiliated Hospital of Southern Medical University, Guangzhou 510630, China.

出版信息

Nan Fang Yi Ke Da Xue Xue Bao. 2021 Oct 20;41(10):1588-1592. doi: 10.12122/j.issn.1673-4254.2021.10.20.

Abstract

OBJECTIVE

To investigate the role of G-protein coupled receptor Smoothened (Smo) in regulating proliferation and migration of adult neural stem cells (ANSCs) and explore the underlying mechanism.

METHODS

Cultured ANSCs were treated with purmorphamine (PM, an agonist of Smo) or cyclopamine (CPM, an inhibitor of Smo), and the changes in cell proliferation migration abilities were assessed using cell counting kit-8 (CCK8) assay and wound healing assay, respectively. The mRNA expressions of membrane receptor Patched 1 (Ptch1), Smo, glioma-associated oncogene homolog 1 (Gli1), axon guidance cue slit1 (Slit1) and brain-derived neurotrophic factor (BDNF) in the treated cells were detected using real-time quantitative PCR (RT-PCR).

RESULTS

PM significantly promoted the proliferation ( < 0.01) and migration of ANSCs ( < 0.01), and up-regulated the mRNA expressions of Ptch1, Smo, Gli1, Slit1 and BDNF. Treatment with CPM significantly inhibited the proliferation and migration of ANSCs.

CONCLUSION

Modulating Smo activity can positively regulate the proliferation and migration of ANSCs possibly by regulating the expressions of BDNF and Slit1.

摘要

目的

探讨G蛋白偶联受体Smoothened(Smo)在调节成年神经干细胞(ANSCs)增殖和迁移中的作用,并探究其潜在机制。

方法

用嘌呤胺(PM,Smo激动剂)或环杷明(CPM,Smo抑制剂)处理培养的ANSCs,分别采用细胞计数试剂盒-8(CCK8)法和划痕愈合试验评估细胞增殖迁移能力的变化。采用实时定量PCR(RT-PCR)检测处理后细胞中膜受体Patched 1(Ptch1)、Smo、胶质瘤相关癌基因同源物1(Gli1)、轴突导向因子slit1(Slit1)和脑源性神经营养因子(BDNF)的mRNA表达。

结果

PM显著促进ANSCs的增殖(<0.01)和迁移(<0.01),并上调Ptch1、Smo、Gli1、Slit1和BDNF的mRNA表达。CPM处理显著抑制ANSCs的增殖和迁移。

结论

调节Smo活性可能通过调节BDNF和Slit1的表达来正向调节ANSCs的增殖和迁移。

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