Soluble Forms of the Receptor for Advanced Glycation Endproducts (RAGE) in Periodontitis
Soluble Forms of the Receptor for Advanced Glycation Endproducts (RAGE) in Periodontitis
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DOI：
10.1038/s41598-019-44608-2
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发表时间：
2019-06-03
影响因子：
4.6
通讯作者：
Lalla, Evanthia
中科院分区：
文献类型：
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作者：
Detzen, Laurent;Cheng, Bin;Lalla, Evanthia
晚期糖基化终末产物 (RAGE) 受体在慢性炎症性疾病的病理学中发挥着重要作用。 RAGE 的可溶形式已被提议作为炎症和代谢状况严重程度以及监测治疗反应的生物标志物。本研究的目的是确定牙周炎中可溶性 RAGE 的循环水平，并评估牙龈组织中细胞结合的全长 RAGE 及其拮抗剂 AGER1 的局部表达。包括牙周炎患者和牙周健康、性别和年龄匹配的对照组（每组 50 名）。牙周炎患者的血清总可溶性 RAGE 和裂解 RAGE (cRAGE) 水平显着降低。两组的内源性分泌型 esRAGE 水平相似。经过多次调整后，牙周炎组的 cRAGE 仍显着较低，并且与体重指数和所有牙周参数呈统计学上显着的负相关。在牙周炎患者中，与健康牙龈相比，受牙周炎影响的牙龈组织中全长 RAGE 和 AGER1 的基因表达显着较高。 RAGE的可溶形式，特别是cRAGE，可以作为牙周炎的存在和严重性/程度的生物标志物，并且可能涉及其发病机制及其作为全身炎症应激源的作用。
The receptor for advanced glycation endproducts (RAGE) is critically involved in the pathobiology of chronic inflammatory diseases. Soluble forms of RAGE have been proposed as biomarkers of severity in inflammatory and metabolic conditions, and in monitoring therapeutic responses. The aim of the present study was to determine circulating levels of the soluble forms of RAGE in periodontitis and to evaluate the expression of cell-bound, full-length RAGE and its antagonist AGER1 locally, in gingival tissues. Periodontitis patients and periodontally healthy, sex- and age-matched controls (50 per group) were included. Serum levels of total soluble RAGE and cleaved RAGE (cRAGE) were significantly lower in periodontitis patients. Levels of the endogenous secretory esRAGE were similar in the two groups. cRAGE remained significantly lower in the periodontitis group following multiple adjustments, and had a statistically significant inverse correlation with body mass index and all periodontal parameters. In periodontitis patients, gene expression of full-length RAGE and of AGER1were significantly higher in periodontitis-affected gingival tissues compared to healthy gingiva. Soluble forms of RAGE, particularly cRAGE, may serve as biomarkers for the presence and severity/extent of periodontitis, and may be implicated in its pathogenesis and its role as a systemic inflammatory stressor.