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

IF 2 3区医学 Q2 DENTISTRY, ORAL SURGERY & MEDICINE

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

摘要

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。

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

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.