衰老改变了阿迪波涅克受体对骨髓衍生中介细胞干细胞信号传递的影响
Hanghang Liu1,2, Qiucheng Zhao1,3, Shibo Liu1
1State Key Laboratory of Oral Diseases & National Center for Stomatology & National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan, China.
Aging cell
|October 28, 2024
概括
衰老会改变阿迪波涅克受体的信号传递,对年轻和老年小鼠的骨修复产生不同的影响. 在年轻小鼠中,AdipoRon促进了骨愈合,但由于与年龄相关的途径变化,在老年小鼠中阻碍了骨愈合.
科学领域:
- 内分泌学和骨生物学 骨生物学
- 细胞和分子医学是细胞和分子医学.
背景情况:
- 阿迪波涅丁受体信号传递是潜在的治疗点,用于与年龄相关的疾病,如骨质疏松症.
- 由于复杂的调节机制和受体变异性,在骨质稳定和骨折修复中的阿迪波内克丁的作用上存在相互矛盾的文献.
研究的目的:
- 在年轻小鼠和老年小鼠中,研究ponektin受体信号传递对骨髓中介质干细胞的差异效应.
- 阐明底层的分子机制与年龄相关调节的阿迪波内克丁受体通路.
主要方法:
- 单细胞测序和体内染色以分析老老鼠骨髓中的阿迪波涅克丁受体表达.
- 在年轻和年老的小鼠中用阿迪波涅克丁受体激活剂 (AdipoRon) 治疗,以评估骨再生和修复.
- 针对AdipoRon治疗的下游信号通路 (Wnt,MAPK,mTOR,NF-κB,AKT) 的反应分析.
主要成果:
- 年龄较大的小鼠表现出ponektin受体表达的改变 (较高的AdipoR2,较低的AdipoR1) 和ponektin水平的增加.
- 在年轻小鼠中,AdipoRon增强了骨修复,但在老年小鼠中损害了它,诱导衰老并抑制骨质生成.
- 在年轻小鼠和老鼠的AdipoRon治疗细胞中观察到Wnt,MAPK和mTOR通路的差异激活.
结论:
- 衰老显著调节骨髓中介质干细胞中的ponektin受体信号传递.
- 受体转录,分布和下游途径激活的变化有助于对阿迪波涅克受体激动剂的年龄相关反应.
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