Frizzled-9触发了actin聚合,并激活了机械传感器YAP,以拯救模拟的微重力诱导的骨质细胞功能障碍
Qiusheng Shi1, Jinpeng Gui1, Lianwen Sun1
1Key Laboratory of Biomechanics and Mechanobiology (Beihang University), Ministry of Education, Beijing Advanced Innovation Center for Biomedical Engineering, School of Biological Science and Medical Engineering, Beihang University, Beijing, China.
Frizzled-9 (Fzd9) 蛋白质有助于骨细胞在模拟的微重力条件下发挥作用. 过度表达Fzd9通过促进乙聚合和YES相关蛋白 (YAP) 核转移来拯救骨质细胞功能障碍,这表明Fzd9是太空飞行引起的骨损失的治疗标.
科学领域:
- 太空生物学空间生物学
- 细胞生物学 细胞生物学
- 生物化学 生物化学
背景情况:
- 长期太空飞行会导致骨质损失和骨质母细胞功能障碍.
- Frizzled-9 (Fzd9) 是一个Wnt受体,对骨质母细胞分化和骨形成至关重要.
研究的目的:
- 调查Fzd9在模拟微重力 (SMG) 诱导的骨质细胞功能障碍中的作用.
- 探索涉及Fzd9在骨细胞功能中的潜在分子机制.
主要方法:
- 骨质细胞暴露于SMG1-7天.
- 在后肢卸载后,Fzd9表达在体外和大鼠大腿骨中进行了分析.
- 使用Fzd9过度表达来评估其对骨质生成标记物和信号通路的影响.
- 西方涂抹和免疫光被用来研究蛋白质表达和局部化.
主要成果:
- SMG降低了骨质生成标志物 (ALP,OPN,RUNX2) 和Fzd9表达.
- 过度表达Fzd9挽救了SMG诱导的骨质生殖标志物的下降.
- 过度表达Fzd9促进了F-actin聚合,YAP的核转位,并调节了Akt/ERK酸化.
- SMG对pGSK3β和β-catenin的影响没有受到Fzd9过度表达的调节.
结论:
- Fzd9对SMG诱导的骨质母细胞功能障碍起着保护作用.
- 通过触发actin聚合和激活YAP,Fzd9挽救了骨质细胞的功能.
- Fzd9是太空飞行引起的骨损失和其他骨疾病的潜在治疗点.
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