CircPVT1 promotes periodontitis progression by regulating miR-24-3p/HIF1AN pathway.

IF 2.2 3区医学 Q2 Dentistry

Journal of Stomatology Oral and Maxillofacial Surgery Pub Date : 2025-02-20 DOI:10.1016/j.jormas.2024.102198

Yuting Bian, Jingwen Yu, Yang Liu, Yahong Shi, Yujiao Hou, Xin Liu

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引用次数: 0

Abstract

Purpose and background: Periodontitis is a chronic inflammatory oral disease affecting half of the adult population. Circular RNA plays a critical role in periodontitis. CircPVT1(hsa_circ_0085536) was abundant in periodontitis tissues and cells but its mechanism are still unclear. We aim to explore the role of circPVT1 in periodontitis and elucidate how circPVT1 acts.

Methods: Gingival tissues from patients with periodontitis(n=20) and health participants(n=20) were collected and the expression of circPVT1 was measured by realtime quantitative PCR(RT-qPCR). Cell model for periodontitis was performed by PDLCs treated lipopolysaccharide(LPS). Cell Counting Kit-8(CCK-8), flow cytometry, enzyme-linked immunoabsorbent assay (ELISA), ALP staining and Alizarin red staining were conducted to detect cell viability, apoptosis, inflammatory and oxidative stress factors and osteogenic differentiation. The targeting microRNA(miRNA)/mRNA axis of circPVT1 was predicted and screened.

Results: circPVT1 was upregulated in the gingival tissues of patients with periodontitis. Silencing of circPVT1 inhibited cell viability, decreased inflammatory factors(IL-1β, TNF-α, IL-6) and oxidative stress factors, activated NRF-2 and HO-1 expression and promoted apoptosis and osteoclast differentiation in PDLCs after treated LPS. However, these effects were reversed by transfected miR-24-3p inhibitor and overexpressed of hypoxia-inducible factor 1 subunit alpha inhibitor(HIF1AN) in PDLCs.

Conclusion: circPVT1 promotes the progression of periodontitis by modulating NRF-2/HO-1 pathway via the miR-24-3p/HIF1AN axis.

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CircPVT1通过调节miR-24-3p/HIF1AN通路促进牙周炎进展。

目的和背景：牙周炎是一种影响半数成年人的慢性口腔炎症性疾病。环状RNA在牙周炎中起着关键作用。CircPVT1（has_circ_0085536）在牙周炎组织和细胞中大量存在，但其作用机制尚不清楚。我们旨在探讨circPVT1在牙周炎中的作用，并阐明circPVT1的作用机制。方法：收集20例牙周炎患者（n=20）和健康受试者（n=20）的牙龈组织，采用实时定量PCR（RT-qPCR）检测circPVT1表达。采用脂多糖（LPS）处理的pdlc建立牙周炎细胞模型。采用细胞计数试剂盒-8（CCK-8）、流式细胞术、酶联免疫吸附法（ELISA）、ALP染色和茜素红染色检测细胞活力、凋亡、炎症和氧化应激因子及成骨分化。预测和筛选circPVT1的靶向microRNA(miRNA)/mRNA轴。结果：circPVT1在牙周炎患者牙龈组织中表达上调。沉默circPVT1抑制细胞活力，降低炎症因子（IL-1β、TNF-α、IL-6）和氧化应激因子，激活NRF-2和HO-1表达，促进LPS处理后pdlc细胞凋亡和破骨细胞分化。然而，通过转染miR-24-3p抑制剂和在pdlc中过表达缺氧诱导因子1亚单位α抑制剂（HIF1AN），这些作用被逆转。结论：circPVT1通过miR-24-3p/HIF1AN轴调控NRF-2/HO-1通路促进牙周炎的进展。

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

Journal of Stomatology Oral and Maxillofacial Surgery Dentistry-Oral Surgery

CiteScore

2.20

自引率

9.10%

发文量

305

期刊介绍： J Stomatol Oral Maxillofac Surg publishes research papers and techniques - (guest) editorials, original articles, reviews, technical notes, case reports, images, letters to the editor, guidelines - dedicated to enhancing surgical expertise in all fields relevant to oral and maxillofacial surgery: from plastic and reconstructive surgery of the face, oral surgery and medicine, … to dentofacial and maxillofacial orthopedics. Original articles include clinical or laboratory investigations and clinical or equipment reports. Reviews include narrative reviews, systematic reviews and meta-analyses. All manuscripts submitted to the journal are subjected to peer review by international experts, and must: Be written in excellent English, clear and easy to understand, precise and concise; Bring new, interesting, valid information - and improve clinical care or guide future research; Be solely the work of the author(s) stated; Not have been previously published elsewhere and not be under consideration by another journal; Be in accordance with the journal''s Guide for Authors'' instructions: manuscripts that fail to comply with these rules may be returned to the authors without being reviewed. Under no circumstances does the journal guarantee publication before the editorial board makes its final decision. The journal is indexed in the main international databases and is accessible worldwide through the ScienceDirect and ClinicalKey Platforms.