由M2巨细胞表达的TGF-β通过抑制中细胞干细胞TSG-6表达来促进伤口愈合
Young Woo Eom1, Ju-Eun Hong2, Pil Young Jung3
1Regeneration Medicine Research Center, Yonsei University Wonju College of Medicine, Wonju, Korea.
PloS one
|April 21, 2025
概括
在伤口愈合过程中,M2巨细胞减少了由脂肪组织衍生干细胞 (ASC) 产生的瘤缩因子-α (TNF-α) 刺激的6基因 (TSG-6) 生产. 这一过程由转化生长因子-β (TGF-β) 介导,最终增强了伤口的修复.
科学领域:
- 细胞生物学 细胞生物学
- 免疫学 免疫学 免疫学
- 再生医学是一种再生医学.
背景情况:
- 伤口愈合需要协调的细胞和分子相互作用.
- 瘤亡因子-α (TNF-α) 刺激的基因6 (TSG-6) 是组织修复的重要调节者.
- 脂肪组织衍生干细胞 (ASC) 和巨细胞在伤口愈合中起着至关重要的作用.
研究的目的:
- 调查ASC在伤口愈合期间对M2巨细胞的反应中对TSG-6产生的调节.
- 阐明转化生长因子-β (TGF-β) 和TNF-α在这个过程中的作用.
主要方法:
- 同时培养M2巨细胞和ASCs.
- 对TSG-6,TGF-β和TNF-α表达水平的分析.
- 在LX-2细胞中评估伤口关闭和纤维化反应.
主要成果:
- 干白素 (IL) - 4/IL-13在ASC中诱导TSG-6,但M2巨细胞降低了它.
- M2巨体表现出增加的TGF-β和减少的TNF-α.
- TGF-β抑制了ASCs的IL-4/IL-13-诱导的TSG-6产生.
- TSG-6抑制了TGF-β诱导的伤口关闭和纤维化反应.
- 来自M2巨细胞的TGF-β阻止了TSG-6的产生,促进了伤口愈合.
结论:
- 伤口微环境中的TNF-α和TGF-β平衡调节ASC TSG-6的产生,调节愈合过程.
- 针对TNF-α/TGF-β平衡提供了增强伤口修复和减少纤维化的潜在治疗策略.
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