Related Experiment Video
Updated: May 8, 2026
Inducing Apical Periodontitis in Mice
Published on: August 6, 2019
miR-455-3p is Involved in the Pathological Mechanism of Pulpitis by Modulating ACTG1
Yuejing Xu1, Yihan Fu2, Lei Zhang3
1Department of Stomatology, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, China.
Background:
Pulpitis is an inflammatory condition primarily induced by bacteria. The onset of pulpitis is typically accompanied by severe pain, which seriously affects the life quality of patients. miR-455-3p was identified to be abnormally expressed in multiple conditions and participated in disease progression. Nevertheless, the action of miR-455-3p on pulpitis is unknown.
Aim:
To dig out a novel biomarker for the diagnosis of pulpitis and to elaborate the related molecular mechanisms.
Methods:
qRT-PCR was employed to examine the levels of miR-455-3p and ACTG1 in serum, tissues and cells. Dual-luciferase reporter assay was utilized to validate the targeting relationship. CCK-8 assay was applied to check cell proliferation. Flow cytometry analysis was designed to monitor apoptosis.
Results:
The miR-455-3p levels were significantly reduced in serum and tissue of pulpitis patients. ROC curve analysis revealed that miR-455-3p had good diagnostic performance for pulpitis. In vitro, miR-455-3p levels were inversely proportional to LPS concentration and treatment time. And LPS treatment suppressed the proliferation. Moreover, up-regulated miR-455-3p facilitated proliferation and repressed apoptosis. Down-regulated miR-455-3p depressed proliferation and induced apoptosis. Mechanistically, ACTG1 is a target gene of miR-455-3p and negatively regulated by miR-455-3p. Upregulating miR-455-3p attenuated the suppression of proliferation and promotion of apoptosis by LPS, which could be further reversed by overexpressing ACTG1.
Conclusion:
miR-455-3p may serve as a novel diagnostic biomarker for pulpitis. And miR-455-3p could enhance proliferation and restrain apoptosis by negatively regulating ACTG1.
Insights
MicroRNA-455-3p (miR-455-3p) is a potential diagnostic biomarker for pulpitis. This study found that miR-455-3p enhances cell proliferation and inhibits apoptosis by regulating ACTG1, offering insights into pulpitis mechanisms.
Area of Science:
- Biochemistry
- Molecular Biology
- Dental Research
Background:
- Pulpitis, an inflammatory condition caused by bacteria, leads to severe pain and reduced quality of life.
- MicroRNA-455-3p (miR-455-3p) is implicated in various diseases, but its role in pulpitis remains unclear.
Purpose of the Study:
- To identify a novel biomarker for pulpitis diagnosis.
- To elucidate the molecular mechanisms underlying pulpitis involving miR-455-3p.
Main Methods:
- Quantitative real-time PCR (qRT-PCR) to measure miR-455-3p and ACTG1 levels.
- Dual-luciferase reporter assay to confirm targeting.
- Cell Counting Kit-8 (CCK-8) assay for proliferation analysis.
- Flow cytometry for apoptosis assessment.
Main Results:
- miR-455-3p levels were significantly decreased in pulpitis patients' serum and tissues.
- ROC curve analysis indicated good diagnostic performance for miR-455-3p in pulpitis.
- In vitro studies showed miR-455-3p levels inversely correlated with LPS concentration and treatment time, with LPS suppressing proliferation.
- Upregulated miR-455-3p promoted proliferation and inhibited apoptosis, while downregulated miR-455-3p had opposite effects.
- ACTG1 was identified as a direct target of miR-455-3p, negatively regulated by it. Upregulating miR-455-3p counteracted LPS-induced effects, an effect reversed by ACTG1 overexpression.
Conclusions:
- miR-455-3p shows promise as a novel diagnostic biomarker for pulpitis.
- miR-455-3p enhances proliferation and suppresses apoptosis in pulpitis by negatively regulating ACTG1.
Related Concept Videos
01:10Mechanism of Angiogenesis
01:24Regulation of Angiogenesis and Blood Supply
01:16TGF - β Signaling Pathway