细胞外矩阵的刚性通过重编程脂肪酸氧化依赖的巨细胞极化来促进神经元的外生长
Shan Wang1, Xu Chu2, Zhaoyang Liu3
1Department of Urology, The First Affiliated Hospital of ZhengZhou University, Zheng Zhou 450052, China; Department of Biomedical Engineering, Faculty of Engineering, The Hong Kong Polytechnic University, Hong Kong, China.
Biochimica et biophysica acta. General subjects
|November 24, 2024
概括
细胞外矩阵的刚性会影响免疫细胞的行为,促进免疫抑制性巨细胞,帮助组织修复. 这一发现为伤口愈合和神经发生提供了新的治疗途径.
科学领域:
- 生物材料科学 生物材料科学
- 免疫学 免疫学 免疫学
- 组织工程是组织工程.
背景情况:
- 细胞外基质 (ECM) 在组织修复和再生中起着至关重要的作用.
- 单细胞分化为巨细胞,对伤口愈合至关重要,但ECM硬性的影响尚不清楚.
研究的目的:
- 研究细胞外矩阵 (ECM) 刚度对单细胞分化和巨细胞功能的影响.
- 探索ECM度影响巨细胞两极化的潜在机制.
主要方法:
- 开发了具有不同硬度的生物相容的凝-基烯酸酸水凝.
- 在不同硬度的水凝上利用了巨细胞培养.
- 进行了与脂肪酸氧化 (FAO) 相关的代谢物分析和评估蛋白质表达.
主要成果:
- 高基质刚度诱导了免疫抑制性巨细胞表型,增加了IL-10,TGF-β,CD206和CD163的表达.
- 刚性水凝调高了与粮农组织相关的蛋白质 (PPAR-γ,PPAR-δ),推动了免疫抑制的分化.
- 鉴定出4-基酸是关键的上调代谢物,可以提供对炎症的保护.
结论:
- ECM度是巨细胞偏向免疫抑制表型的关键调节者.
- 针对ECM硬性和相关的代谢途径 (FAO) 是提高组织修复的有希望的策略.
- 由基质刚度调节的巨细胞极化可以促进临床组织再生应用.
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