关键词: Autophagy Ras-associated binding proteins microRNA periodontitis pyroptosis

来  源:   DOI:10.4103/jisp.jisp_179_23   PDF(Pubmed)

Abstract:
UNASSIGNED: The intricate interplay between periodontal polymicrobial flora and an altered immune response is the central cause of periodontal disease. Multiple cell death methods and their interactions, along with the associated signaling pathways, significantly impact the initiation and advancement of periodontitis. Our speculation revolves around the role of the miR-223/Ras-associated binding protein (RAB12) signaling axis in regulating autophagy-induced pyroptosis, contributing to the pathophysiology of periodontitis. Thus, this study aimed to investigate miR-223 and RAB12 expression patterns in Stage III/Grade B periodontal disease.
UNASSIGNED: The study included 50 healthy individuals and 50 patients diagnosed with Stage III/Grade B periodontal disease. Clinical parameters were cataloged for each participant. miRNA-223 underwent an in silico analysis to identify its potential target genes. Gingival crevicular fluid (GCF) samples were collected from the subjects for real-time polymerase chain reaction to evaluate the expression of both miR-223 and the RAB12 gene.
UNASSIGNED: The miRTargetLink2.0 analysis highlighted the RAB12 gene as a prime target for miR-223. In periodontal disease patients, miR-223 and RAB12 gene expressions significantly increased (15.21 and 34.70-fold changes, respectively; P < 0.05). Receiver operating characteristic analysis suggested that miR-223 is a potential biomarker for periodontal disease, with 76% diagnostic accuracy and an area under the curve of 0.777 (P < 0.01).
UNASSIGNED: MicroRNA-223 and its target gene RAB12 exhibit high expression levels in GCF samples from individuals with periodontal disease. This suggests modulation of autophagy and the signaling mechanism for pyroptotic cell death in periodontal tissues during pathogenesis. Consequently, the miR-223/RAB12 axis might represent a plausible link for periodontal disease.
摘要:
牙周微生物菌群与改变的免疫反应之间的复杂相互作用是牙周疾病的主要原因。多种细胞死亡方法及其相互作用,以及相关的信号通路,显著影响牙周炎的发生和进展。我们的推测围绕miR-223/Ras相关结合蛋白(RAB12)信号轴在调节自噬诱导的焦凋亡中的作用。有助于牙周炎的病理生理学。因此,本研究旨在探讨miR-223和RAB12在III期/B级牙周病中的表达模式。
该研究包括50名健康个体和50名诊断为III期/B级牙周病的患者。对每个参与者的临床参数进行编目。miRNA-223进行了计算机模拟分析以鉴定其潜在的靶基因。从受试者收集龈沟液(GCF)样品用于实时聚合酶链反应,以评估miR-223和RAB12基因的表达。
miRTargetLink2.0分析突出显示RAB12基因作为miR-223的主要靶标。在牙周病患者中,miR-223和RAB12基因表达显著增加(15.21和34.70倍变化,分别;P<0.05)。受试者工作特性分析表明miR-223是牙周病的潜在生物标志物,诊断准确率为76%,曲线下面积为0.777(P<0.01)。
MicroRNA-223及其靶基因RAB12在来自患有牙周病的个体的GCF样品中表现出高表达水平。这表明在发病过程中牙周组织中自噬的调节和细胞凋亡的信号机制。因此,miR-223/RAB12轴可能代表了牙周病的合理联系.
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