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巨细胞衍生的细胞外囊泡调节骨干/祖细胞血统命运和肥胖的骨恶化

Chen He¹, Chen Hu¹, Wen-Zhen He¹

¹Department of Endocrinology, Endocrinology Research Center, Xiangya Hospital of Central South University, Changsha, Hunan, 410008, China.

Bioactive materials

|July 29, 2024

概括

肥胖会通过改变含有microRNA的巨细胞外细胞囊泡 (EVs) 而导致骨质恶化,然后破坏骨干干细胞的分化. 操纵这些EV可以逆转骨质损失,提供治疗潜力.

科学领域:

生物医学科学生物医学科学
细胞生物学细胞生物学
干细胞研究干细胞研究

背景情况:

肥胖引起的慢性炎症会对组织健康和干细胞功能产生负面影响.
肥胖对骨组织的具体影响和潜在的机制在很大程度上是未知的.

研究的目的:

研究肥胖如何通过巨细胞分泌的细胞外囊泡 (EVs) 影响骨干/原生细胞 (SSPCs).
为了确定参与肥胖引起的骨质恶化和探索治疗干预的microRNAs.

主要方法:

从肥胖和瘦小鼠的骨髓巨细胞 (BMM) 分泌的细胞外囊泡 (EVs) 的比较分析.
将BMM-EV给接受者小鼠,以评估对骨健康的影响.
在肥胖的BMM-EV中对差异表达的microRNA的查和功能验证.
基因操纵 (有条件淘汰/过度表达) 关键的微RNAs 在小鼠.
开发用于向microRNA治疗的aptamer工程EV传递系统.

主要成果:

来自肥胖小鼠的BMM-EV诱导了瘦小鼠的骨恶化,而来自瘦小鼠的EV改善了肥胖小鼠的骨健康.
确定了miR-140和miR-378a作为SSPC分化的关键调节剂,准Pparα-Abca1轴.
条件淘汰miR-140防止了肥胖引起的骨质恶化,而SSPC中的过度表达导致了骨质损失.
在BMM中miR-378a的耗尽导致了类似肥胖的骨质恶化.
针对性地输送miR-378a-3p过载的BMM-EV,在肥胖小鼠中挽救了骨质恶化.

结论:

携带特定微RNA的巨细胞衍生的EV在调解肥胖引起的骨质恶化方面发挥着关键作用.
在BMM-EV中,miR-140和miR-378a的平衡决定了SSPC的命运和骨稳定.
基于EV的微RNA的向输送为与肥胖相关的骨疾病提供了一个有前途的治疗策略.

关键词:

亚普特美尔 (Aptamer) 是一种药物.细胞命运细胞命运细胞特异性向针对性巨细胞衍生的细胞外囊泡.肥胖引起的骨质恶化骨干细胞/原始细胞

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