CircPVT1 promotes periodontitis progression by regulating miR-24-3p/HIF1AN pathway - 07/03/25

Doi : 10.1016/j.jormas.2024.102198

Yuting Bian ^a,^{^{1
These two authors contributed equally to this work.}}, Jingwen Yu ^b,^{^{1
These two authors contributed equally to this work.}}, Yang Liu ^a, Yahong Shi ^a, Yujiao Hou ^c, Xin Liu ^d,^⁎
^a Department of Stomatology, Second Hospital of Shijiazhuang, Shijiazhuang, Hebei, 050000, PR China
^b The Affiliated Stomatological Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, 330006, PR China
^c Department of Stomatology, Affiliated Hospital of Hebei University, Baoding, Hebei, 071000, PR China
^d Department of Stomatology, The Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050017, PR China

^⁎Corresponding author at: 12 Health Road, Shijiazhuang, Hebei 050017, PR China.12 Health RoadShijiazhuangHebei050017PR China

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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.