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<p>Pulpitis is an inflammatory disease affecting the dental pulp tissue, impacting patients’ oral health and daily life. MicroRNAs (miRNAs) are involved in the progression of pulpitis. This study aims to elucidate the regulatory role of the miR-140-3p/ACSL1 axis in pulpitis, particularly its molecular mechanisms within dental pulp cells. The levels of miR-140-3p and long-chain acyl CoA synthetase 1 (ACSL1) was measured by RT-qPCR. The receiver operating characteristic (ROC) curve represented the diagnostic capability of miR-140-3p. Lipopolysaccharide (LPS) derived from Escherichia coli was applied to mimic pulp tissue inflammation in vitro. Inflammatory markers were tested via ELISA. Bioinformatics tools predicted miR-140-3p target sites. Target relationships were validated by dual-luciferase reporter assay. The expression of miR-140-3p was downregulated in inflamed pulp tissue, and it could distinguish between healthy individuals and pulpitis patients. In vitro, the miR-140-3p mimic enhanced proliferation and superoxide dismutase (SOD) activity while reducing apoptosis and the levels of interleukin-6 (IL-6), interleukin-1β (IL-1β), and malondialdehyde (MDA) in LPS-treated hDPCs. These situations were abolished by ACSL1. In conclusion, low levels of miR-140-3p were involved in the progression of pulpitis. By negatively regulating ACSL1, miR-140-3p promotes proliferation while suppressing apoptosis, inflammation, and oxidative stress, thereby alleviating pulpitis.</p>

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Dysregulation of miR-140-3p is involved in the pathogenesis of pulpitis via the regulation of ACSL1

  • 期刊论文

  • 发表日期：

    2026年1月10日

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  • Shuhua Li,
  • Hongzhong Ding

摘要

Pulpitis is an inflammatory disease affecting the dental pulp tissue, impacting patients’ oral health and daily life. MicroRNAs (miRNAs) are involved in the progression of pulpitis. This study aims to elucidate the regulatory role of the miR-140-3p/ACSL1 axis in pulpitis, particularly its molecular mechanisms within dental pulp cells. The levels of miR-140-3p and long-chain acyl CoA synthetase 1 (ACSL1) was measured by RT-qPCR. The receiver operating characteristic (ROC) curve represented the diagnostic capability of miR-140-3p. Lipopolysaccharide (LPS) derived from Escherichia coli was applied to mimic pulp tissue inflammation in vitro. Inflammatory markers were tested via ELISA. Bioinformatics tools predicted miR-140-3p target sites. Target relationships were validated by dual-luciferase reporter assay. The expression of miR-140-3p was downregulated in inflamed pulp tissue, and it could distinguish between healthy individuals and pulpitis patients. In vitro, the miR-140-3p mimic enhanced proliferation and superoxide dismutase (SOD) activity while reducing apoptosis and the levels of interleukin-6 (IL-6), interleukin-1β (IL-1β), and malondialdehyde (MDA) in LPS-treated hDPCs. These situations were abolished by ACSL1. In conclusion, low levels of miR-140-3p were involved in the progression of pulpitis. By negatively regulating ACSL1, miR-140-3p promotes proliferation while suppressing apoptosis, inflammation, and oxidative stress, thereby alleviating pulpitis.