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Parto Babaniamansour¹, Diego Jacho¹, Agustin Rabino²

¹Department of Bioengineering, College of Engineering, University of Toledo, Toledo, OH, United States.

Frontiers in immunology

|January 24, 2025

概括

将TRPV4抑制与6%的机械应变相结合,有效地将促炎性巨细胞转移到抗炎状态,促进组织愈合和炎症解决.

科学领域:

生物医学工程生物医学工程
细胞生物学细胞生物学
免疫学免疫学免疫学

背景情况:

巨细胞两极分化对于解决炎症和使组织修复至关重要.
瞬态受体潜在化物4 (TRPV4) 通道是调节巨细胞表型的潜在目标.
机械负荷 (机械疗法) 可以影响细胞行为和炎症反应.

研究的目的:

研究机械应变和TRPV4抑制对巨细胞两极分化的联合作用.
为了确定诱导抗炎性巨细胞表型的最佳机械负荷参数.
探索这种综合方法在促进炎症解决方面的潜力.

主要方法:

在3D原基质中培养出促炎症 (M1) 巨细胞.
在0%,3%和6%的振幅下施加机械应变.
使用RN-1734 (10μM) 的TRPV4抑制.
通过基因表达,蛋白质分析 (免疫组织化学) 和细胞外矩阵活性评估巨细胞表型.

主要成果:

3%的机械应变增加了促炎性标记物和蛋白质分解活性.
在3%的菌株中,TRPV4抑制部分降低了炎症.
6%的机械菌株与TRPV4抑制抑制了MAPK信号传递,减少了促炎基因,增加了抗炎标志物 (例如CD206).
免疫组织化学证实了CD80/CD206表达的转变,表明两极分化向抗炎状态.

结论:

与6%的机械应变相结合的TRPV4抑制有效诱导一种抗炎性巨细胞表型.
这种方法对调节炎症微环境有希望.
这些发现表明,增强组织修复和炎症解决的潜在治疗策略.

关键词:

抗炎症的表型抗炎症的表型抑制,机械负荷的增加.巨细胞的两极分化基激活蛋白激酶 (MAPK) 是一种激活蛋白激酶.促炎性 (M1) 巨细胞三维 (3D) 原基质矩阵暂时受体潜在化物4 (TRPV4)

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