微小RNA（MicroRNAs）在尖周牙周炎的发病中发挥了作用。先前在尖周牙周炎样本中报告了miR-10a-5p 的上调和 miR-891a-5p 的下调。本研究旨在对miR-10a-5p 进行功能性特征化研究，探究其调节炎性细胞因子和生长因子表达的能力以及在尖周牙周炎的发展中可能存在的与miR-891a-5p 共调控机制。将miR-10a-5p mimic/对照和miR-891a-5p 抑制剂/对照引入人K-562细胞中，存在或不存在脂多糖的情况下进行实验。通过定量逆转录聚合酶链反应检验细胞裂解液中的靶基因，并对细胞裂解液进行蛋白质组分析。此外，还共转染 miR-10a-5p mimics 和 miR-891a-5p 抑制剂到K-562细胞中。进行RNA测序和定量逆转录聚合酶链反应以检验它们的靶基因。miR-10a-5p 的过表达导致肿瘤坏死因子α和白细胞介素1β mRNA 的下调以及转化生长因子β 1（TGFB1）mRNA 的上调表达，而白细胞介素3和 TGF-β1 蛋白则上调。同时过表达miR-10a-5p 和抑制miR-891a-5p 进一步增加了 TGFB1 mRNA 转录水平。RNA测序揭示，miR-10a-5p 和 miR-891a-5p 共调控的基因可能涉及尖周牙周炎相关的通路，如肿瘤坏死因子、瞬时受体电位和血管内皮生长因子信号通路。miR-10a-5p 可能调节多种炎性细胞因子和生长因子的表达，如肿瘤坏死因子α、IL-1β、白细胞介素3和TGF-β1。此外，miR-10a-5p 和 miR-891a-5p 协同调节 TGFB1 基因表达，并且这种共调控的基因网络与尖周牙周炎中的许多通路相集成。版权所有 © 2023 美国根管治疗医师协会。由 Elsevier 公司出版。保留所有权利。

MicroRNAs have been shown to play a role in the pathogenesis of apical periodontitis. Upregulation of miR-10a-5p and downregulation of miR-891a-5p were previously reported in apical periodontitis samples. This study aims to perform a functional characterization of miR-10a-5p, investigating its capacity to regulate the expression of inflammatory cytokines and growth factors, as well as a possible co-regulation mechanism with miR-891a-5p in the development of apical periodontitis.miR-10a-5p mimics/controls and miR-891a-5p inhibitors/controls were introduced to human K-562 cells in the presence or absence of lipopolysaccharide. Total RNA was extracted from cell lysates, and target genes were examined via quantitative reverse transcription-polymerase chain reaction. Cell lysates were also subjected to proteomics analysis. Furthermore, mimics of miR-10a-5p and inhibitors of miR-891a-5p were co-transfected into K-562 cells. RNA sequencing and quantitative reverse transcription-polymerase chain reaction were carried out to examine their target genes.Overexpression of miR-10a-5p led to downregulation of tumor necrosis factor-alpha and interleukin-1 beta mRNA and upregulation of transforming growth factor-beta 1 (TGFB1) mRNA expression, whereas interleukin 3 and TGF-β1 proteins were upregulated. Simultaneous overexpression of miR-10a-5p and inhibition of miR-891a-5p further increased TGFB1 mRNA transcript levels. RNA sequencing revealed that genes co-regulated by miR-10a-5p and miR-891a-5p may be involved in apical periodontitis-related pathways such as tumor necrosis factor, transient receptor potential, and vascular endothelial growth factor signaling pathways.miR-10a-5p may modulate the expression of multiple inflammatory cytokines and growth factors such as tumor necrosis factor-alpha, IL-1β, interleukin 3, and TGF-β1. In addition, miR-10a-5p and miR-891a-5p cooperatively regulate TGFB1 gene expression, and the gene network of this co-regulation is integrated with many pathways in apical periodontitis.Copyright © 2023 American Association of Endodontists. Published by Elsevier Inc. All rights reserved.