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S100A4 在人根尖肉芽肿发病机制中的作用。

Role of S100A4 in the Pathogenesis of Human Periapical Granulomas.

机构信息

Department of Endodontics, Nihon University School of Dentistry, Tokyo, Japan.

Nihon University Graduate School of Dentistry, Dental Research Center, Tokyo, Japan.

出版信息

In Vivo. 2021 Jul-Aug;35(4):2099-2106. doi: 10.21873/invivo.12479.

DOI:10.21873/invivo.12479
PMID:34182485
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8286529/
Abstract

BACKGROUND/AIM: S100A4 expression is associated with the pathology of chronic inflammatory diseases. In this study, we investigated the role of S100A4 and four inflammatory mediators (IL-1β, IκB, IL-10, and TNF-α) in human periapical granulomas (PGs).

MATERIALS AND METHODS

S100A4 expression in PGs obtained by apicoectomy was examined by immunohistochemistry. Further, the expression of S100A4 and four inflammatory mediators was compared between PGs and healthy gingival tissues (HGTs) using real-time PCR.

RESULTS

In the PGs, S100A4 was found to be expressed in endothelial cells and fibroblasts. Furthermore, real-time PCR revealed that the expression of S100A4 and IL-1β in PGs was significantly higher than that in HGTs. Although a correlation between the expression of S100A4 and IκB or IL-10 was not detected, a positive correlation between the expression of S100A4 and IL-1β or TNF-α was observed.

CONCLUSION

The expression of S100A4 correlates with the pathogenesis of PGs.

摘要

背景/目的:S100A4 的表达与慢性炎症性疾病的病理学有关。在这项研究中,我们研究了 S100A4 和四种炎症介质(IL-1β、IκB、IL-10 和 TNF-α)在人根尖肉芽肿(PGs)中的作用。

材料和方法

通过根尖切除术获得的 PGs 中的 S100A4 表达通过免疫组织化学进行检查。此外,使用实时 PCR 比较 PGs 和健康牙龈组织(HGTs)中 S100A4 和四种炎症介质的表达。

结果

在 PGs 中,发现 S100A4 在血管内皮细胞和成纤维细胞中表达。此外,实时 PCR 显示 PGs 中 S100A4 和 IL-1β 的表达明显高于 HGTs。虽然未检测到 S100A4 表达与 IκB 或 IL-10 之间的相关性,但观察到 S100A4 表达与 IL-1β 或 TNF-α 之间呈正相关。

结论

S100A4 的表达与 PGs 的发病机制相关。

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NF-κB, IκB, and IKK: Integral Components of Immune System Signaling.NF-κB、IκB 和 IKK:免疫系统信号的重要组成部分。
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Extracellular S100A4 negatively regulates osteoblast function by activating the NF-κB pathway.细胞外S100A4通过激活NF-κB信号通路负向调控成骨细胞功能。
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Induction of S100A4 in periodontal ligament cells enhances osteoclast formation.牙周膜细胞中S100A4的诱导增强破骨细胞形成。
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S100A4-neutralizing antibody suppresses spontaneous tumor progression, pre-metastatic niche formation and alters T-cell polarization balance.S100A4中和抗体可抑制肿瘤自发进展、前转移生态位形成并改变T细胞极化平衡。
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The metastasis-associated protein S100A4 promotes the inflammatory response of mononuclear cells via the TLR4 signalling pathway in rheumatoid arthritis.转移相关蛋白 S100A4 通过 TLR4 信号通路促进类风湿关节炎中单核细胞的炎症反应。
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