在模拟的微重力条件下,SphK1通过促进糖分解来抑制人类牙髓干细胞亡
Jingyi Che1,2, Zhengjun Qiu1,2, Huailong Hou1,2
1Department of Endodontics, First Affiliated Hospital of Harbin Medical University, Harbin, China, hrbmu.edu.cn.
Journal of tissue engineering and regenerative medicine
|December 22, 2025
概括
模拟的微重力增强糖解并减少人类牙纸干细胞 (hDPSCs) 的亡. 这种效应是由斯芬哥辛激酶1 (SphK1) 的上调调节介导,促进干细胞的存活.
科学领域:
- 太空生命科学 太空生命科学
- 干细胞生物学 干细胞生物学
- 细胞代谢细胞代谢
背景情况:
- 甘油分解对于介酶干细胞 (MSC) 的增殖和生存至关重要.
- 微重力对MSC新陈代谢和亡的影响尚未完全理解.
- 研究模拟微重力对人类牙纸干细胞 (hDPSC) 的影响对于空间生物学来说很重要.
研究的目的:
- 为了研究模拟微重力 (SMG) 对hDPSCs的糖溶性活性和亡的影响.
- 阐明神素激酶1 (SphK1) 在调解这些效应中的作用.
- 在SMG下证实糖解对亡的保护作用.
主要方法:
- 通过乳酸和葡萄糖测量评估糖分流.
- 使用qPCR和蛋白质表达 (HK2,PKM2) 通过西式涂抹量化基因表达 (HK2,PKM2,LDHA).
- 使用附件V-FITC/PI染色和免疫阻塞对与亡相关的蛋白质 (BAX,BCL-2,割裂caspase-3) 进行评估的亡.
- 使用药理抑制剂 (用于SphK1的PF-543,用于糖解的2-DG).
主要成果:
- 在hDPSC中,SMG显著增加了糖分分解能力,并降低了apoptosis.
- 在SMG下,SphK1的表达被上调,其抑制减弱了糖解和抗质效应.
- 通过2-DG抑制糖解,增加了亡,证实了糖解的保护作用.
- 这些发现突出了SphK1作为一个关键的调节器,将增强的糖解与SMG下减少的亡联系起来.
结论:
- 模拟的微重力增强糖解和抑制hDPSC中的亡,部分通过SphK1上调.
- 微重力条件可能促进干细胞的生存和功能.
- 准糖解路径和SphK1可能有助于保持干细胞在太空环境中的生存能力.
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