与年龄相关的对MSC免疫调节,巨细胞极化,亡和骨再生的影响与IL-38表达相关
Jiewen Zhang1, Kentaro Akiyama1, Aung Ye Mun1
1Department of Oral Rehabilitation and Regenerative Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama 700-8558, Japan.
International journal of molecular sciences
|March 28, 2024
概括
衰老会损害介质干细胞 (MSC) 和它们与巨细胞的相互作用,延迟骨愈合. MSCs促进巨细胞亡和M2极化,但这在老年小鼠中减少了.
科学领域:
- 免疫学 免疫学 免疫学
- 再生医学是一种再生医学.
- 骨生物学 骨生物学
背景情况:
- 介酶干细胞 (MSC) 调节免疫反应,帮助组织修复.
- 巨细胞与MSC的相互作用对于骨愈合至关重要,但尚未完全理解.
- 与年龄相关的MSC功能下降可能会影响免疫细胞调节.
研究的目的:
- 研究MSCs与年龄相关的损伤如何影响它们在骨愈合过程中与巨细胞的相互作用.
- 在年轻小鼠和老年小鼠中阐明MSC-巨细胞通信的机制.
主要方法:
- 利用年轻和老年小鼠模型进行骨愈合研究.
- 采用免疫涂层来分析MSC和M1巨细胞的时空定位.
- 进行了体外共同培养实验,以研究MSC-巨相互作用和调节机制.
主要成果:
- 老年小鼠表现出延迟的骨愈合,M1巨细胞增加和愈合部位的MSCs减少.
- 在体外,MSCs通过可溶性因子诱导M1亡,并通过可溶性因子抑制促炎性细胞因子.
- MSCs在M1巨细胞中调高了Interleukin-38 (IL-38),这促进了M2极化并抑制了M1亡.
结论:
- MSCs的免疫调节作用,包括M1亡和M2极化,随着年龄的增长而减弱,延迟骨愈合.
- 在老年小鼠中减少的MSC数量和功能会损害M1巨细胞清除和炎症解决.
- M1衍生的IL-38在组织再生期间在免疫调节中发挥作用.
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