胰岛素通过减弱IIS/PI3K/AKT/mTOR通路轴来促进人类牙纸干细胞的骨形成能力
Lingling E1, Yanbo Shan1, Yuxi Luo1
1Institute of Stomatology & Oral Maxilla Facial Key Laboratory, First Medical Center of Chinese PLA General Hospital, Beijing, China.
Stem cell research & therapy
|July 29, 2024
概括
胰岛素通过诱导胰岛素耐药性和降低IIS/PI3K/AKT/mTOR通路的调节,促进牙髓干细胞的增殖和骨形成. 这项研究澄清了胰岛素.
科学领域:
- 干细胞生物学 干细胞生物学
- 内分泌学 在内分泌学.
- 生物材料科学 生物材料科学
背景情况:
- 胰岛素在骨代谢中的作用已确立,但其在牙髓干细胞 (DPSCs) 增殖和骨质分化的精确分子机制尚不清楚.
- 了解胰岛素对DPSC的影响对于再生牙科和骨组织工程至关重要.
研究的目的:
- 研究胰岛素对人类DPSCs骨形成能力的影响.
- 阐明胰岛素对DPSCs影响的分子机制,重点关注胰岛素信号通路.
主要方法:
- 使用CCK-8测定和细胞表型通过流细胞计评估DPSC增殖.
- 使用染色方法评估差异化潜力 (托洛伊丁蓝色,油红色O,阿利沙林红色,阿尔西安蓝色).
- 量化基因和蛋白质表达 (RT-qPCR,西式涂抹),分析骨标记物,并在体内 (小鼠,子) 评估骨再生.
主要成果:
- 胰岛素显著增强了DPSC的扩散和矿化基质的形成,以剂量依赖的方式.
- 10−6 M胰岛素上调了骨质生成标志物,并在体内促进了骨的形成.
- 胰岛素通过降低IIS/PI3K/AKT/mTOR通路的调节诱导胰岛素耐药性,正如改变的酸化状态和抑制剂研究所证明的那样.
结论:
- 胰岛素促进了DPSC的扩散,骨质分化和骨的形成.
- 这种效应是由诱导胰岛素耐药性和随后的IIS/PI3K/AKT/mTOR途径下调调的介导.
- 这些发现为使用胰岛素和DPSCs的骨再生提供了新的治疗策略的见解.
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