SFRP1通过MAPK信号通路对牙髓干细胞活性及血管生成的机制研究

The Mechanism of SFRP1 on the Activity and Angiogenesis of Dental Pulp Stem Cells through MAPK Signaling Pathway

目的:探究牙髓干细胞的分子调控机制。方法:购买人源牙髓干细胞(DPSC),转染si-NC/SFRP1至DPSC,qRT-PCR和Westernblot检测SFRP1的表达。CCK-8、流式细胞术检测各组细胞的增殖活力及凋亡情况。细胞划痕实验、管状形成实验检测各组细胞的迁移、血管形成能力变化。Westernblot检测MAPK信号通路关键蛋白p-p38、p38的蛋白变化。结果:敲低DPSC中SFRP1的表达后,DPSC的增殖活力下降,凋亡率显著增多;细胞的迁移能力及血管形成能力显著下降;MAPK信号通路中p-p38的蛋白含量显著降低。结论:敲低SFRP1通过失活MAPK信号通路抑制牙髓干细胞的增殖活力、血管生成能力,促进其凋亡。

Objective:To explore the molecular regulation mechanism of dental pulp stem cells.Methods:Human dental pulp stem cells(DPSC)were purchased and transfected with si-NC/SFRP1.The mRNA and protein expression level of SFRP1 was detected by qRT-PCR and Western blot.CCK-8 and flow cytometry were used to detect the proliferation activity and apoptosis of cells in each group.Cell wound healing and angiogenesis assays were used to detect the changes of cell migration and angiogenesis ability in each group.Western blot was used to detect the protein changes of p-p38 and p38 in MAPK signaling pathway.Results:After knocking down the expression of SFRP1 in DPSC,the proliferation activity of DPSC decreased and the apoptosis rate increased significantly.Cell migration and angiogenesis ability decreased significantly;the protein content of p-p38 in MAPK signaling pathway was significantly decreased.Conclusion:Knockdown of SFRP1 inhibited the proliferation and angiogenesis of dental pulp stem cells and promoted their apoptosis by inactivating the MAPK signaling pathway.