纤维细胞生长因子23通过自信号通路调节缺氧诱导的骨质细胞亡
Qipu Yin1, Hongxia Yang2, Lun Fang1
1Institute of Sports Medicine, Shandong First Medical University and Shandong Academy of Medical Sciences, Taian, Shandong 271016, P.R. China.
Molecular medicine reports
|September 15, 2023
概括
纤维细胞生长因子23 (FGF23) 通过向microRNA-17-5p并激活自,促进缺氧诱导的骨质细胞亡. 这表明FGF23是潜在的骨髓缩治疗点.
科学领域:
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
- 生物化学 生物化学
背景情况:
- 缺氧是骨质细胞亡和骨髓缩的关键因素.
- 了解缺氧诱导的骨质细胞死亡的分子机制对于开发有效的治疗方法至关重要.
研究的目的:
- 研究纤维细胞生长因子23 (FGF23) 在缺氧诱导的骨质细胞亡中的作用和机制.
- 在这个过程中探索FGF23,microRNA-17-5p (miR-17-5p) 和自之间的关系.
主要方法:
- 在初级骨质母细胞和MC3T3-E1细胞中建立低氧诱导的亡细胞模型.
- 通过RT-qPCR和西式涂抹对FGF23表达的分析.
- 使用MTT测定,染色,流细胞计和基因表达分析评估亡和自标志物.
- 路西法酶记者分析证实了FGF23和miR-17-5p之间的准关系.
主要成果:
- FGF23显著降低了骨质细胞存活率和增加了亡.
- 观察到对亡基因 (Bax,caspases 3/9) 的上调和对抗亡基因 (Bcl-2) 的下调.
- 与自相关的蛋白质 (贝克林-1,LC3-II) 的表达增加表明了自激活.
- 证实FGF23直接针对miR-17-5p,miR-17-5p的抑制逆转了FGF23沉默效应.
结论:
- FGF23促进缺氧诱导的骨质细胞亡,可能通过准miR-17-5p和调节自信号通路.
- 这些发现突出了FGF23作为一种潜在的治疗点,用于诸如股骨头骨硬化等疾病.
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