摘要
背景:神经前体细胞的细胞周期调控是神经发生和发展的基本过程,并且能够修复脑外伤。周所周知基质细胞衍生因子-1(SDF-1,CXCL12)及其受体CXCR4 和 CXCR7能很好调节NPCs的迁移和存活。CXCL12对NPCs的增殖、细胞周期调控及其相关联的信号通路的影响还待研究。细胞周期蛋白在NPCs中的细胞周期调控、增殖以及存活起到非常关键的作用。 方法:原代小鼠神经前体细胞源于在胚胎13.5天时野生型、敲除CXCR4基因或敲除CXCR7基因的脑组织。流式细胞术通过检测DNA含量来分析细胞周期。实时PCR和免疫印迹分别用来评估mRNA和蛋白的表达。Ki67免疫染色和原位末端标记分析试验分别用来估测mNPCs的增殖和存活。 结果:CXCL12预处理引起了G0/G1期的缩短和S期的增长,表明CXCL12调控mNPCs的细胞周期过程。同样,CXCL12治疗增加了细胞周期蛋白和β-联蛋白的表达,提高了mNPCs的增殖和存货。mNPCs中CXCR7基因的敲除阻碍了CXCL12介导的mNPCs的增殖,然而CXCR4的敲除没有明显影响CXCL12介导的mNPCs的增殖。
关键词: 神经前体细胞;细胞周期;细胞周期蛋白;凋亡
Current Molecular Medicine
Title:CXCR7 Participates in CXCL12-mediated Cell Cycle and Proliferation Regulation in Mouse Neural Progenitor Cells
Volume: 16 Issue: 8
Author(s): Y. Wang, P. Xu, L. Qiu, M. Zhang, Y. Huang, J.C. Zheng
Affiliation:
关键词: 神经前体细胞;细胞周期;细胞周期蛋白;凋亡
摘要: Background: Cell cycle regulation of neural progenitor cells (NPCs) is an essential process for neurogenesis, neural development, and repair after brain trauma. Stromal cell-derived factor-1 (SDF-1, CXCL12) and its receptors CXCR4 and CXCR7 are well known in regulating the migration and survival of NPCs. The effects of CXCL12 on NPCs proliferation, cell cycle regulation, and their associated signaling pathways remain unclear. Cyclin D1 is a protein required for progression through the G1 phase of the cell cycle and a known downstream target of β -catenin. Therefore, cyclin D1 plays critical roles of cell cycle regulation, proliferation, and survival in NPCs.
Methods: Primary mouse NPCs (mNPCs) were derived from brain tissues of wild-type, Cxcr4 knockout, or Cxcr7 knockout mice at mouse embryonic day 13.5 (E13.5). Flow cytometry was used to perform cell cycle analysis by quantitation of DNA content. Real-time PCR and Western blot were used to evaluate mRNA and protein expressions, respectively. Ki67 immunostaining and TUNEL assay were used to assess the proliferation and survival of mNPCs, respectively.
Results: CXCL12 pretreatment led to the shortening of G0/G1 phase and lengthening of S phase, suggesting that CXCL12 regulates cell cycle progression in mNPCs. Consistently, CXCL12 treatment increased the expression of CyclinD1 and β -catenin, and promoted proliferation and survival of mNPCs. Cxcr7 knockout of mNPCs blocked CXCL12-mediated mNPCs proliferation, whereas Cxcr4 knockout mNPC did not significantly effect CXCL12- mediated mNPCs proliferation.
Conclusion: CXCR7 plays an important role in CXCL12-mediated mNPC cell cycle regulation and proliferation.
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Cite this article as:
Y. Wang, P. Xu, L. Qiu, M. Zhang, Y. Huang, J.C. Zheng , CXCR7 Participates in CXCL12-mediated Cell Cycle and Proliferation Regulation in Mouse Neural Progenitor Cells, Current Molecular Medicine 2016; 16 (8) . https://dx.doi.org/10.2174/1566524016666160829153453
DOI https://dx.doi.org/10.2174/1566524016666160829153453 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
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