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失调的S100A9表达损害了慢性伤口中的矩阵沉积

Sandra Franz¹, Marta Torregrossa¹, Ulf Anderegg¹

¹Department of Dermatology, Venereology and Allergology, Max Bürger Research Centre, Medical Faculty, University Leipzig, Johannisallee 30, 04103 Leipzig, Germany.

International journal of molecular sciences

|September 28, 2024

概括

过度表达的S100A9蛋白质会损害慢性伤口中的细胞外基质 (ECM) 沉积. 在糖尿病伤口模型中阻断S100A9恢复了ECM功能,表明S100A9是慢性伤口愈合的治疗点.

科学领域:

生物医学科学生物医学科学
伤口治愈研究研究伤口治愈研究
分子生物学分子生物学

背景情况:

慢性不愈合的伤口表现出持续的炎症和受损的细胞外基质 (ECM) 合成.
在延迟伤口愈合时,S100A8/A9蛋白质失调,影响免疫细胞功能.

研究的目的:

在受损伤愈合模型中调查S100A9过度表达在纤维细胞ECM功能中的病理作用.
探索S100A9作为慢性伤口治疗的潜在治疗点.

主要方法:

使用db/db小鼠 (糖尿病模型) 和铁过载小鼠 (慢性静脉腿模型).
分析了S100A8/A9表达,ECM沉积和伤口组织中的炎症媒介.
研究了S100A9对纤维细胞ECM功能通过托尔类受体4 (TLR4) 信号传递的作用机制.
评估了阻断S100A9在db/db小鼠伤口中的治疗效果.

主要成果:

两种小鼠模型都显示了伤口关闭的延迟,持续的炎症和ECM沉积的减少,反映了人类的慢性伤口.
在这些模型和人类慢性伤口中,延长S100A8和S100A9表达与受损的ECM沉积相关.
发现S100A9通过TLR4依赖信号直接改变纤维细胞ECM蛋白和酶表达.
在db/db小鼠中阻断S100A9恢复了纤维细胞ECM功能和增加了矩阵沉积.

结论:

失调的S100A9直接导致慢性伤口中ECM沉积受损.
在影响纤维细胞ECM功能方面,S100A9扮演着未知的病理作用.
在慢性伤口中,S100A9代表了增强组织修复的有希望的治疗标.

关键词:

在S100A8A8中使用.在S100A9A9中使用.慢性伤口慢性伤口糖尿病糖尿病患者糖尿病患者细胞外矩阵是细胞外矩阵.纤维细胞的细胞.铁过载是什么?铁过载是什么?

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