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PI3K/AKT/mTOR信号调节BCP陶诱导的骨质发生

Peijie Tan¹, Yuchen Hua¹, Bo Yuan¹

¹National Engineering Research Center for Biomaterials, Sichuan University, No. 29 Wangjiang Road, Chengdu 610064, China. qzeng8156@scu.edu.cn.

Journal of materials chemistry. B

|July 10, 2024

概括

双相酸 (BCP) 陶通过激活介酶干细胞中的PI3K/AKT/mTOR信号传递,促进骨再生. 抑制这种途径会阻断BCP诱导的骨形成和血管生长.

科学领域:

生物材料科学生物材料科学
再生医学是一种再生医学.
细胞信号传递细胞信号传递

背景情况:

已知双相酸 (BCP) 陶可以诱导骨再生.
在BCP介导骨质生成的基础上,精确的分子机制尚不清楚.

研究的目的:

调查PI3K/AKT/mTOR信号通路在BCP陶诱导骨质生成中的作用.
阐明BCP陶如何影响介质干细胞行为和骨形成.

主要方法:

用BCP陶培养了来自小鼠骨髓的介质干细胞 (BMSCs).
使用选择性阻断剂可以抑制PI3K,AKT和mTOR信号通路.
分析了基因表达 (OPN,RUNX2,VEGF) 和蛋白质酸化.
在小鼠肌内植入后,BCP陶植入物在体内被评估.

主要成果:

BCP陶以时间依赖的方式促进了BMSC的扩散.
在BMSC中,BCP陶激活了PI3K/AKT/mTOR信号通路.
抑制PI3K/AKT/mTOR信号消除了BCP诱导的骨质分化和血管生成.
阻止这种途径减少了干细胞透和新的骨形成 in vivo.

结论:

PI3K/AKT/mTOR信号通路是BCP陶诱导骨质生成的一个关键调节器.
BCP陶利用这种途径来增强骨再生和血管化.
准PI3K/AKT/mTOR信号可能为使用BCP生物材料的骨修提供治疗策略.

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