PI3K/AKT/mTOR通路
运行x2
化学
SOX2
蛋白激酶B
细胞生物学
染色质免疫沉淀
间质细胞
间充质干细胞
信号转导
内科学
转录因子
生物
医学
生物化学
基因表达
发起人
基因
作者
Li Gan,Yu Li,Min Jiang,Xuemei Luo,Fen Wang,Jing Zhao
标识
DOI:10.1016/j.ejphar.2022.174954
摘要
It is reported that the osteogenesis in bone marrow mesenchymal stem cells (BMSCs) can alleviate osteoporosis progression. It has been found that Kae can promote the osteogenesis in BMSCs. However, the mechanism by which Kae mediates the osteogenesis in BMSCs is largely unknown.RBMSCs were collected from rats. The cytotoxicity of Kae was detected by CCK-8 assay. The osteogenic calcification in rBMSCs was measured by alizarin red staining, and ALP staining was performed to test the ALP activity in rBMSCs. The binding relationship between SOX2 and miR-124-3p was explored by dual luciferase report assay and Chromatin Immunoprecipitation (ChIP). RT-qPCR and western blot were performed to assess mRNA and protein levels, respectively.Kae (10 μM) significantly increased the calcification, ALP activity, SOX2 level, activated PI3K/Akt/mTOR signaling and inhibited miR-124-3p level in rBMSCs, while knockdown of SOX2 reversed this phenomenon. Meanwhile, SOX2 suppressed the transcription of miR-124-3p, and SOX2 promoted the osteogenic differentiation in rBMSCs via regulation of miR-124-3p. MiR-124-3p could inactivate PI3K/Akt/mTOR to inhibit the osteogenic differentiation.Kae significantly promoted the osteogenesis in rBMSCs via mediation of SOX2/miR-124-3p/PI3K/Akt/mTOR axis. Thus, our study might shed new lights in exploring new methods against osteoporosis.
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