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牙龈卟啉单胞菌抑制 microRNA-205-5p 的表达可调节牙龈上皮细胞中的促炎细胞因子。

Porphyromonas gingivalis Inhibition of MicroRNA-205-5p Expression Modulates Proinflammatory Cytokines in Gingival Epithelial Cells.

机构信息

Department of Stomatology, Yantai Yuhuangding Hospital, Zhifu District, No. 20 Yuhuangding East Road, Yantai, 264000, Shandong, China.

出版信息

Biochem Genet. 2020 Aug;58(4):566-579. doi: 10.1007/s10528-020-09957-y. Epub 2020 Apr 17.

Abstract

In this study, we strived to investigate the effect of miR-205-5p on JAK/STAT signaling way induced by P. gingivalis in periodontitis. Microarray analysis was conducted to find differentially expressed miRNAs in periodontitis patients. The miRNAs related to JAK/STAT signaling way were selected via DIANA TOOLS, and the targeted mRNAs of miRNAs were predicted by TargetScan. The expression of miRNAs and mRNAs, differentially expressed in periodontitis and related to JAK/STAT signaling, was detected by qRT-PCR or western blot. The relationship between miRNAs and mRNAs was confirmed by a dual luciferase assay. MiR-205-5p was downregulated and IL6ST was upregulated in periodontitis patients' clinical samples. MiR-205-5p had target binding sites of IL6ST 3' untranslated region. QRT-PCR and western blot analysis demonstrated poor expression of miR-205-5p, while IL6ST, pJAK2, p-STAT3 were extremely upregulated in gingival epithelial cells (GECs) with P. gingivalis induction. IL6ST expression in periodontitis tissue was also increased. P. gingivalis could inhibit miR-205-5p expression to activate JAK/STAT signaling in GECs and promote the occurrence and development of periodontitis.

摘要

在这项研究中,我们致力于研究 miR-205-5p 对牙周炎中 P. gingivalis 诱导的 JAK/STAT 信号通路的影响。通过微阵列分析寻找牙周炎患者中差异表达的 miRNAs。通过 DIANA TOOLS 选择与 JAK/STAT 信号通路相关的 miRNAs,通过 TargetScan 预测 miRNAs 的靶向 mRNAs。通过 qRT-PCR 或 Western blot 检测与 JAK/STAT 信号相关的差异表达的 miRNAs 和 mRNAs 的表达。通过双荧光素酶测定验证 miRNA 和 mRNAs 之间的关系。在牙周炎患者的临床样本中,miR-205-5p 下调,IL6ST 上调。miR-205-5p 在 IL6ST 3'UTR 中有靶结合位点。QRT-PCR 和 Western blot 分析表明,牙龈上皮细胞(GECs)中 miR-205-5p 表达水平降低,而 IL6ST、pJAK2、p-STAT3 表达水平极度升高,在 P. gingivalis 诱导下。牙周炎组织中 IL6ST 的表达也增加了。P. gingivalis 可以抑制 miR-205-5p 的表达,从而激活 GECs 中的 JAK/STAT 信号通路,并促进牙周炎的发生和发展。

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