Circ_0062491 alleviates LPS-induced apoptosis and inflammation in periodontitis by regulating miR-498/SOCS6 axis

IF 2.8 4区医学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Innate Immunity Pub Date : 2022-06-09 DOI:10.1177/17534259211072302

Lie Wang, Yanli Li, Feifei Hong, Haiyan Ning

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引用次数: 3

Abstract

Periodontitis is a prevalent chronic inflammatory disease. Circular RNAs (circRNAs) have been revealed to play roles in the inflammatory response. Hence, this work aimed to explore the role and mechanism of circ_0062491 in periodontitis progression. Human periodontal ligament cells (PDLCs) were isolated from the periodontal ligament (PDL) of the healthy teeth with orthodontic requirement after tooth extraction. In vitro experiments were conducted by cell counting Kit-8 (CCK-8) assay, flow cytometry, Western blot, and ELISA to determine cell viability, apoptosis, and inflammatory response. The binding between miR-498 and circ_0062491 or SOCS6 was confirmed using dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Circ_0062491 expression was decreased in periodontitis and LPS-induced PDLCs. Restoration of circ_0062491 attenuated LPS-induced apoptosis and inflammation in PDLCs in vitro. Mechanistically, circ_0062491 functioned as a sponge for miR-498, and miR-498 directly targeted SOCS6. Rescue experiments showed that miR-498 up-regulation reversed the protective action of circ_0062491 on PDLCs under LPS treatment. Moreover, silencing of miR-498 protected PDLCs from LPS-induced apoptosis and inflammation, which were abolished by SOCS6 knockdown. Circ_0062491 protected PDLCs from LPS-induced apoptosis and inflammation, suggesting a new target for the amelioration of periodontitis patients.

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Circ_0062491通过调节miR-498/SOCS6轴减轻LPS诱导的牙周炎细胞凋亡和炎症

牙周炎是一种常见的慢性炎症性疾病。环状核糖核酸（circRNAs）已被揭示在炎症反应中发挥作用。因此，本工作旨在探索circ_0062491在牙周炎进展中的作用和机制。从有正畸需求的健康牙齿的牙周膜（PDL）中分离出人牙周膜细胞（PDLC）。通过细胞计数试剂盒-8（CCK-8）测定、流式细胞术、蛋白质印迹和ELISA进行体外实验，以确定细胞活力、细胞凋亡和炎症反应。miR-498与circ_0062491或SOCS6之间的结合使用双荧光素酶报告子和RNA免疫沉淀（RIP）测定得到证实。Circ_0062491在牙周炎和LPS诱导的PDLC中的表达降低。circ_0062491的恢复在体外减弱了LPS诱导的PDLC中的细胞凋亡和炎症。从机制上讲，circ_0062491充当miR-498的海绵，miR-498直接靶向SOCS6。救援实验表明，miR-498的上调逆转了circ_0062491在LPS处理下对PDLC的保护作用。此外，miR-498的沉默保护PDLC免受LPS诱导的细胞凋亡和炎症的影响，这些作用被SOCS6敲低所消除。Circ_0062491保护PDLC免受LPS诱导的细胞凋亡和炎症的影响，为改善牙周炎患者提供了一个新的靶点。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Innate Immunity 生物-免疫学

CiteScore

7.20

自引率

0.00%

发文量

审稿时长

6-12 weeks

期刊介绍： Innate Immunity is a highly ranked, peer-reviewed scholarly journal and is the official journal of the International Endotoxin & Innate Immunity Society (IEIIS). The journal welcomes manuscripts from researchers actively working on all aspects of innate immunity including biologically active bacterial, viral, fungal, parasitic, and plant components, as well as relevant cells, their receptors, signaling pathways, and induced mediators. The aim of the Journal is to provide a single, interdisciplinary forum for the dissemination of new information on innate immunity in humans, animals, and plants to researchers. The Journal creates a vehicle for the publication of articles encompassing all areas of research, basic, applied, and clinical. The subject areas of interest include, but are not limited to, research in biochemistry, biophysics, cell biology, chemistry, clinical medicine, immunology, infectious disease, microbiology, molecular biology, and pharmacology.