Knockdown of MALAT1 Inhibits the Progression of Chronic Periodontitis via Targeting miR-769-5p/HIF3A Axis.
Knockdown of MALAT1 Inhibits the Progression of Chronic Periodontitis via Targeting miR-769-5p/HIF3A Axis.
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DOI：
10.1155/2021/8899863
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发表时间：
2021
影响因子：
--
通讯作者：
Ge H
中科院分区：
文献类型：
--
作者：
Chen Q;Cao M;Ge H
慢性牙周炎（CP）是一种严重影响口腔健康的长期炎症性疾病。本研究旨在探讨转移相关肺腺癌转录本1（MALAT1）在慢性牙周炎中的调控机制。
采用牙龈卟啉单胞菌脂多糖（LPS）处理原代人牙周膜细胞（PDLCs）以建立慢性牙周炎模型。实时定量聚合酶链反应（qRT - PCR）用于检测慢性牙周炎患者牙龈组织以及LPS处理的PDLCs中MALAT1和miR - 769 - 5p的表达。采用3 -（4,5 - 二甲基 - 2 - 噻唑基）- 2,5 - 二苯基 - 2 - H - 四氮唑溴盐（MTT）法检测细胞活力。酶联免疫吸附测定（ELISA）用于检测炎症细胞因子水平。通过蛋白质印迹法测定半胱天冬酶 - 3、Bax、Bcl - 2和缺氧诱导因子（HIF）3A的蛋白水平。应用双荧光素酶报告基因（DLR）实验验证miR - 769 - 5p与MALAT1/HIF3A之间的靶标关系。
在慢性牙周炎患者牙龈组织以及LPS处理的PDLCs中，MALAT1和HIF3A的表达增强，而miR - 769 - 5p的表达降低。MALAT1敲低促进了LPS处理的PDLCs的细胞活力，抑制了炎症和细胞凋亡。MALAT1靶向miR - 769 - 5p并负向调节miR - 769 - 5p的表达。miR - 769 - 5p过表达促进了LPS处理的PDLCs的细胞活力，抑制了炎症和细胞凋亡。此外，miR - 769 - 5p靶向HIF3A并负向调节HIF3A的表达。在体外，miR - 769 - 5p的抑制和HIF3A的过表达均逆转了MALAT1沉默对LPS诱导的PDLC损伤的抑制作用。
MALAT1敲低通过调节miR - 769 - 5p/HIF3A轴减轻了LPS诱导的PDLC损伤，这可能为慢性牙周炎的治疗提供一个新的靶点。
Chronic periodontitis (CP) is a long-lasting inflammatory disease that seriously affects oral health. This study is aimed at investigating the regulatory mechanism of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in CP. Primary human periodontal ligament cells (PDLCs) were treated with P. gingivalis lipopolysaccharide (LPS) to establish a CP model. Quantitative real-time PCR (qRT-PCR) was used to measure the expression of MALAT1 and miR-769-5p in gingival tissues of patients with CP and LPS-treated PDLCs. Cell viability was detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay. Enzyme-linked immunosorbent assay (ELISA) was used to measure the levels of inflammatory cytokines. The protein levels of caspase-3, Bax, Bcl-2, and hypoxia-inducible factor (HIF) 3A were determined by western blot assay. Dual-luciferase reporter (DLR) assay was applied to validate the target relationships between miR-769-5p and MALAT1/HIF3A. The expression of MALAT1 and HIF3A was enhanced, and the expression of miR-769-5p was reduced in gingival tissues of patients with CP and LPS-treated PDLCs. MALAT1 knockdown promoted cell viability and inhibited inflammation and cell apoptosis in LPS-treated PDLCs. MALAT1 targeted miR-769-5p and negatively regulated miR-769-5p expression. miR-769-5p overexpression promoted cell viability and inhibited inflammation and cell apoptosis in LPS-treated PDLCs. Besides, miR-769-5p targeted HIF3A and negatively modulated HIF3A expression. Both miR-769-5p inhibition and HIF3A overexpression reversed the inhibitory effects of MALAT1 silencing on LPS-induced PDLC injury in vitro. MALAT1 knockdown attenuated LPS-induced PDLC injury via regulating the miR-769-5p/HIF3A axis, which may supply a new target for CP treatment.
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影响因子：
4.3
作者：
Shen, Jie;Song, Renduo;Zhao, Hua
通讯作者：
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影响因子：
3.5
作者：
Jin, Su-Han;Zhou, Rui-Hao;Liu, Jian-Guo
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DOI：
10.26355/eurrev_202006_21657
发表时间：
2020-01-01
影响因子：
3.3
作者：
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影响因子：
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作者：
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通讯作者：
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影响因子：
5.2
作者：
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