Overexpression of receptor for advanced glycation end products and high-mobility group box 1 in human dental pulp inflammation.

Overexpression of receptor for advanced glycation end products and high-mobility group box 1 in human dental pulp inflammation.
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DOI:
10.1155/2014/754069
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发表时间:
2014
影响因子:
4.6
通讯作者:
Maruyama I
Maruyama I
中科院分区:
医学3区
文献类型:
--
作者:
Tancharoen S;Tengrungsun T;Suddhasthira T;Kikuchi K;Vechvongvan N;Tokuda M;Maruyama I

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高迁移率组框1 (HMGB1)是一种非组蛋白dna结合蛋白,被释放到细胞外空间并促进炎症。HMGB1结合相关的细胞信号转导受体,包括积极参与血管和炎症疾病的晚期糖基化终产物受体(RAGE)。本研究旨在探讨RAGE和HMGB1是否参与牙髓炎的发病机制,并探讨中间普雷沃氏菌(P. intermedia)脂多糖(LPS)对成牙细胞样细胞(OLC-1)中RAGE和HMGB1表达的影响。临床炎症牙髓中RAGE和HMGB1表达水平高于健康牙髓。RAGE在人牙髓炎组织的成牙髓细胞、间质髓成纤维细胞样细胞和内皮样细胞中表达上调。在成牙细胞中观察到强烈的细胞质HMGB1免疫反应性,而在人牙髓炎组织的髓间质成纤维细胞样细胞中观察到核HMGB1免疫反应性。LPS刺激OLC-1细胞通过RAGE产生HMGB1呈剂量依赖性。抑制NF-κB活化的TPCA-1可抑制HMGB1向细胞质的易位和OLC-1在LPS作用下的分泌。这些结果表明RAGE和HMGB1在牙髓对口腔细菌感染的免疫应答中起重要作用。
High mobility group box 1 (HMGB1), a nonhistone DNA-binding protein, is released into the extracellular space and promotes inflammation. HMGB1 binds to related cell signaling transduction receptors, including receptor for advanced glycation end products (RAGE), which actively participate in vascular and inflammatory diseases. The aim of this study was to examine whether RAGE and HMGB1 are involved in the pathogenesis of pulpitis and investigate the effect of Prevotella intermedia (P. intermedia) lipopolysaccharide (LPS) on RAGE and HMGB1 expression in odontoblast-like cells (OLC-1). RAGE and HMGB1 expression levels in clinically inflamed dental pulp were higher than those in healthy dental pulp. Upregulated expression of RAGE was observed in odontoblasts, stromal pulp fibroblasts-like cells, and endothelial-like cell lining human pulpitis tissue. Strong cytoplasmic HMGB1 immunoreactivity was noted in odontoblasts, whereas nuclear HMGB1 immunoreactivity was seen in stromal pulp fibroblasts-like cells in human pulpitis tissue. LPS stimulated OLC-1 cells produced HMGB1 in a dose-dependent manner through RAGE. HMGB1 translocation towards the cytoplasm and secretion from OLC-1 in response to LPS was inhibited by TPCA-1, an inhibitor of NF-κB activation. These findings suggest that RAGE and HMGB1 play an important role in the pulpal immune response to oral bacterial infection.
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