The Significance of Notch Signaling Pathway in the Differentiation of Rat Bone Mesenchymal Stem Cells Into Schwann Cells
Main Authors: | Dou, Xiaoqin, Zhang, Bei, Wang, Mengyan, Li, Xiaolu, Zhang, Yanxin, Shen, Ruowu |
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Format: | Article eJournal |
Bahasa: | eng |
Terbitan: |
, 2018
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Subjects: | |
Online Access: |
https://zenodo.org/record/3350243 |
Daftar Isi:
- Objective: To investigate the role of Notch signaling pathway in the differentiation of rat bone marrow mesenchymal stem cells (MSCs) into Schwann cells (SCs). Methods: BMSCs were isolated from high glucose medium and cultured in fetal bovine serum (FBS) and α-MEM medium. The resulting cells were treated with β-mercaptoethanol (β-ME), all-trans retinoic acid (RA), platelet-derived factor (PDGF-AA), basic fibroblast growth factor (bFGF), Forskolin, Heregulin .After induction of differentiation,cells were divided into three groups: control group, all-induced group and blocker group. Notch pathway blocker DAPT was added in the blocker group upon induction. The expression of Jagg1 ligand, Hes1 target gene, Notch1, Dll1 receptor protein and signal protein (S100, p75, GFAP) were determined by quantitative RT-qPCR. Cell proliferation was measured by CCK-8. Flow cytometry was used to detect the apoptosis of MSCs .Results: Compared with the control group, the expression of SCs signal protein (S100, p75, GFAP) was significantly increased in the all-induced group and the blocker group. Compared with theall- induced group, the Jagg1 ligand , Hes1 target gene, Notch1, Dll1 receptor protein was significantly lower; compared with the all- induced of the group, the proliferation effect of the blocker group and the apoptosis rate was significantly lower than the other two groups, the difference was statistically significant, P <0.05) . Conclusion: Inhibition of Notch signaling pathway can enhance the differentiation of MSCs into SCs. The possible mechanism is that Notch signaling pathway may promote cell proliferation and promote early apoptosis of MSCs.Read Complete Article at ijSciences: V72018021582 AND DOI: http://dx.doi.org/10.18483/ijSci.1582