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脱氧化亚酸盐通过纤维内克受限吸附抑制巨细胞炎症

Jingxuan Zhou¹, Fanyu Zhang¹, Qinchao Tang¹

¹State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan 430079, China.

Acta biomaterialia

|November 22, 2024

概括

脱氧化酸 (dHAP) 表面通过限制纤维内素吸附和整合素信号传递来减少炎症性巨细胞激活. 这一发现为改善生物相容性和促进组织再生提供了一个新的生物材料策略.

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
表面化学表面化学

背景情况:

巨细胞在异物反应 (FBR) 中发挥着关键作用,影响生物材料的成功.
植入物表面的元素组成会影响生物反应,但机制尚不清楚,特别是关于氧气在巨细胞两极分化中的作用.

研究的目的:

为了研究氧含量对巨细胞激活的影响,使用制造的脱氧化酸 (dHAP) 表面.
阐明植入物接口中的氧气水平调节巨细胞行为的分子机制.

主要方法:

制造脱氧化酸盐 (dHAP) 和酸盐 (HAP) 表面.
对巨细胞激活和炎症反应的分析.
总内部反射显微镜 (TIRFM) 和分子动态 (MD) 模拟用于研究蛋白质吸附和相互作用.

主要成果:

与HAP表面相比,dHAP表面显著抑制了炎症性巨细胞激活.
纤维素 (Fn) 吸附在dHAP上减少,Arg-Gly-Asp (RGD) 活性部位的暴露减少.
减少Fn粘附和RGD识别损害了整合素-焦点粘附激酶 (FAK) 途径,抑制了炎症.

结论:

生物材料接口的氧含量,特别是dHAP,调节蛋白质吸附水平上的巨细胞激活.
降低dHAP表面的纤维内素吸附和整体蛋白信号传递促进了亲再生性巨细胞表型,增强了生物材料的兼容性.

关键词:

纤维纤维素的生长方式异物体反应异物体反应集成, 接口接口巨细胞是一个巨细胞.

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