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内氧硫酸盐通过AhR/Hes1通路抑制骨髓中骨质干细胞的骨质生成

Chin-Wen Hsieh^1,2, Ling-Hua Chang^3,4, Yan-Hsiung Wang^3,4,5

¹Division of Nephrology, Department of Internal Medicine, Pingtung Christian Hospital, Pingtung 900, Taiwan.

International journal of molecular sciences

|August 29, 2024

概括

内氧硫酸盐 (IS) 是一种尿素毒素,它通过通过基碳水化合物受体 (AhR) /Hes1通路抑制骨髓中介酶干细胞 (BMSCs) 的骨质生成,从而损害慢性病 (CKD) 的骨质形成.

科学领域:

腎臟病學 (nephrology) 是一種醫學專業.
骨生物学骨生物学骨生物学
干细胞生物学干细胞生物学

背景情况:

慢性病 (CKD) 与骨疾病,如低循环骨质疏松症有关.
尿素毒素,包括硫酸 (IS),都与骨质形成受损有关.
众所周知,基碳化合物受体 (AhR) 途径抑制骨髓中介质干细胞 (BMSCs) 的骨质基因分化.

研究的目的:

通过AhR/Hes1信号通路调查氧硫酸盐 (IS) 是否影响BMSC骨质生成.
阐明IS影响早期骨形成的分子机制.

主要方法:

培养小鼠BMSCs (D1细胞) 并用不同度的IS.治疗它们.
测量了关键骨质生成基因 (Runx2,Bmp2,Alp,Oc) 的矿化和表达.
评估了AhR和Hes1的表达水平,并利用AhR抗剂和基因淘汰 (Ahr) 来确认途径的参与.

主要成果:

在2-50μM度下,IS显著降低了BMSC矿化和下调的骨质生成基因 (Runx2,Bmp2,Alp,Oc).
通过AhR抗和Ahr敲击,IS对骨质生成的抑制作用被逆转.
通过AhR信号传递,IS诱导了Hes1的表达,导致抑制了Runx2和Bmp2的转录.

结论:

硫酸可以通过激活AhR/Hes1通路来抑制BMSCs的早期骨质生成.
这一途径抑制了关键骨质基因Runx2和Bmp2的转录.
这些发现为CKD患者的骨疾病管理提供了潜在的治疗点.

关键词:

他是他的,他是他的.阿里碳水化合物受体是什么?慢性脏疾病慢性脏疾病硫酸印氧基硫酸盐的使用方法骨质发生过程 (osteogenesis)

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