Dysregulation of Pulpitis Progression Through Modulation of the lncRNA ITGB2-AS1 /miR-1224-5p Axis

通过调控lncRNA ITGB2-AS1/miR-1224-5p轴调控牙髓炎进展

阅读:1

Abstract

INTRODUCTION AND AIMS: The onset of pulpitis is excruciatingly painful, and delayed treatment can lead to serious sequelae. LncRNAITGB2-AS1 is abnormally expressed in pulpitis samples, and thus, the present study was designed to investigate its diagnostic value and regulatory mechanisms in pulpitis. METHODS: RT-qPCR was used to detect the expression of ITGB2-AS1 and miR-1224-5p in 85 cases of pulp tissue and 80 cases of normal tissue. ROC curves were evaluated for the diagnostic value of ITGB2-AS1. Cell proliferation and apoptosis were assayed by the CCK-8 kit and apoptosis kit, respectively. IL-6 and TNF-α levels were measured by ELISA; mRNA levels was assessed by RT-qPCR. SOD and MDA levels were determined using corresponding kits. PPI network analysis identified hub genes among the downstream target genes of miR-1224-5p. RESULTS: Compared with controls, in tissues from patients with pulpitis, ITGB2-AS1 levels were increased and miR-1224-5p levels were decreased. The diagnostic value of ITGB2-AS1 for pulpitis was 0.902, with a high specificity of 92.5%. ITGB2-AS1 can target miR-1224-5p and negatively regulate its expression. Knockout of ITGB2-AS1 significantly improved LPS-impaired cell proliferation, reduced apoptosis, and decreased inflammation and oxidative stress levels. Additionally, MAPK1 is a target of miR-1224-5p. CONCLUSION: ITGB2-AS1 exhibits high diagnostic value for pulpitis patients and holds promise as a novel diagnostic biomarker. Knocking down ITGB2-AS1 targets miR-1224-5p expression, mitigates cellular damage, and restores cellular vitality, thereby potentially slowing pulpitis progression. This establishes a theoretical foundation for positioning ITGB2-AS1 as a future therapeutic target for pulpitis.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。