International dental journal · 2025
miR-455-3p is Involved in the Pathological Mechanism of Pulpitis by Modulating ACTG1.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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Xu Yuejing, Fu Yihan, Zhang Lei
Аннотация
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.
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.