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在β-糖酸盐治疗后,Sirtuin 1在FGF23激活中的作用

Danielle M A Ratsma¹, Max Muller¹, Marijke Koedam¹

¹Laboratory for Calcium and Bone Metabolism and Erasmus MC Bone Centre, Department of Internal Medicine, Erasmus MC, Erasmus University Medical Center, Room Ee585b, Dr. Molewaterplein 40, 3015 GD, Rotterdam, The Netherlands.

Pflugers Archiv : European journal of physiology

|May 21, 2024

概括

酸盐调节涉及影响FGF23的SIRT1-HES1通路,但不是活性氧物种 (ROS). 这项研究阐明了酸盐平衡的FGF23调节机制.

科学领域:

分子生物学分子生物学
细胞生物学细胞生物学
内分泌学在内分泌学.

背景情况:

酸盐稳态对于生物功能至关重要,其破坏会导致有害的健康结果.
纤维细胞生长因子23 (FGF23) 在酸盐调节中起着关键作用,但其上游信号通路,特别是细胞外酸盐传感,需要进一步阐明.
之前的研究表明,反应性氧物种 (ROS) 在FGF23调节中起着作用,但这一点仍需最终确定.

研究的目的:

调查反应性氧物种 (ROS),静音信息调节器1 (SIRT1) 和毛发和增强分裂-1 (HES1) 在FGF23表达的调节中的参与.
阐明细胞外酸盐影响MC3T3-E1细胞FGF23水平的机制.

主要方法:

MC3T3-E1细胞被用β-糖酸盐 (BGP) 治疗,以刺激Fgf23的表达.
通过分别使用NADPH氧化酶抑制剂和 tert-butyl氧化物 (TBHP) 来进行ROS的抑制和诱导.
使用抑制剂Ex527和激活剂SRT1720进行SIRT1活性调节.
在BGP和Ex527治疗后,分析了毛发和Split-1 (HES1) 增强剂的表达水平.

主要成果:

β-糖酸盐 (BGP) 治疗显著增加了MC3T3-E1细胞中的Fgf23表达.
抑制或诱导ROS并没有改变Fgf23表达的BGP介导的增加,这表明ROS没有参与.
抑制SIRT1取消了BGP诱导的Fgf23上调,而SIRT1激活增加了Fgf23的表达.
BGP治疗上调了HES1表达,这种效果因SIRT1抑制而减弱,表明SIRT1-HES1轴参与.

结论:

一个新的SIRT1-HES1信号轴参与了对酸盐的反应中FGF23表达的调节.
在这种细胞模型中,反应性氧物种 (ROS) 似乎在通过酸盐调解FGF23刺激中没有发挥显著作用.
这些发现有助于理解酸盐稳态,并可能为酸盐相关疾病提供潜在的治疗点.

关键词:

纤维细胞生长因子 23 23 营养营养营养营养营养骨质细胞是骨质细胞的组成部分.酸盐是一种酸盐.有反应性氧物种的反应性氧物种.在Sirtuin 11中使用.

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