ArticleOral health & preventive dentistry2023
Dysregulation of MicroRNA-152-3p is Associated with the Pathogenesis of Pulpitis by Modulating SMAD5.
Article in Oral health & preventive dentistry, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed, 2 citations in OpenAlex.
- Dysregulation of miR-140-3p is involved in the pathogenesis of pulpitis via the regulation of ACSL1.Odontology · 2026Article
- Objectively Diagnosing Pulpitis: Opportunities and Methodological Challenges in the Development of Point-of-Care Assays.International journal of molecular sciences · 2025Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeTo research the role of microRNA (miR)-152 in the pathogenesis of pulpitis using a cell model based on human dental pulp cells (HDPCs) treated with lipopolysaccharides (LPS). MATERIALS AND
methodsThe biological activity of HDPCs infected by LPS was measured using a cell counting kit (CCK-8), Transwell test, flow cytometry, and fluorescent quantitative PCR. The concentration of superoxide dismutase (SOD) and malondialdehyde (MDA) was evaluated using an assay kit, the levels of interleukin (IL)-1β and IL-6 were measured by enzyme-linked immunosorbent assay (ELISA), and the targeting relationship between SMAD5 and miR-152 was measured by the double-luciferase report test. The expression of cell cycle-related CyclinD1 and BAX was assessed by PCR. By plotting a receiver operating characteristic (ROC) curve, the diagnostic value of miR-152 was shown.
resultsThe level of miR-152 in HDPCs induced by LPS decreased, while the level of SMAD5 increased. After overexpressing miR-152 in LPS-induced HDPCs, the viability was elevated, the apoptosis rate decreased, CyclinD1 was elevated, BAX diminished, the inflammatory cytokines (IL-6 and IL-1β) were inhibited, the activity of SOD increased, and the MDA content decreased. miR-152 targeted regulation of SMAD5, and SMAD5 modulated the effects of miR-152 on cell viability, apoptosis, inflammation, and the oxidative response of HDPCs. Reduced miR-152 expression was verified in patients with pulpitis, which could be a biomarker for pulpitis.
conclusionmiR-152 was found to be a biomarker correlated with the pathogenesis of pulpitis and the biological behaviour of HDPCs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.