SMURF1 Regulates Periodontal Stem Cell Injury and Osteogenic Differentiation by Regulating TRAF4.

IF 2.9 3区医学 Q1 DENTISTRY, ORAL SURGERY & MEDICINE

Oral diseases Pub Date : 2025-08-01 Epub Date: 2025-04-21 DOI:10.1111/odi.15341

Ziming Wei, Hui Xiao, Lishu Zhou, Yarong Wang

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引用次数: 0

Abstract

Objective: This study aimed to investigate the specific role and mechanistic actions of tumor necrosis factor receptor-associated factor 4 (TRAF4) in periodontitis.

Methods: Human periodontal ligament stem cells (PDLSCs) were exposed to lipopolysaccharide (LPS). Then, real-time quantitative polymerase chain reaction (RT-qPCR) and western blotting (WB) were carried out to determine the mRNA and protein expression levels of Smad ubiquitination regulator 1 (SMURF1). The relationship between TRAF4 and SMURF1, as predicted by the STRING and GeneMANIA databases, was verified by co-immunoprecipitation (Co-IP). Finally, both TRAF4 and SMURF1 were inhibited in PDLSCs by cell transfection, and the regulatory mechanisms involved were investigated by cell counting kit-8 assays, enzyme linked immunosorbent assay, WB, alkaline phosphatase, and alizarin red staining.

Results: The gene and protein expression levels of SMURF1 in PDLSCs increased following LPS induction (p < 0.001); cell viability was decreased (p < 0.001), TRAF4 expression was decreased (p < 0.001), and cell-mineralized nodules were inhibited. Inhibition of SMURF1 expression increased PDLSCs activity and TRAF4 expression levels (p < 0.001), increased the number of cell-mineralized nodules, and enhanced cellular osteogenic capacity (p < 0.001).

Conclusions: SMURF1 regulates LPS-stimulated injury and improves the capacity for osteogenic differentiation in PDLSCs by downregulating the expression of TRAF4.

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SMURF1通过调节TRAF4调控牙周干细胞损伤和成骨分化。

目的：探讨肿瘤坏死因子受体相关因子4 （tumor necrosis factor receptor-associated factor 4, TRAF4）在牙周炎中的具体作用及机制。方法：将人牙周韧带干细胞（PDLSCs）暴露于脂多糖（LPS）中。采用实时定量聚合酶链反应（RT-qPCR）和western blotting （WB）检测Smad泛素化调控因子1 (SMURF1) mRNA和蛋白的表达水平。TRAF4和SMURF1之间的关系，正如STRING和GeneMANIA数据库预测的那样，通过共免疫沉淀（Co-IP）验证。最后，通过细胞转染，TRAF4和SMURF1在PDLSCs中均被抑制，并通过细胞计数试剂盒-8试验、酶联免疫吸附试验、WB、碱性磷酸酶和茜素红染色来研究其调控机制。结果：LPS诱导后，PDLSCs中SMURF1基因和蛋白表达水平升高(p)。结论：SMURF1通过下调TRAF4的表达，调节LPS刺激的损伤，提高PDLSCs成骨分化能力。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Oral diseases 医学-牙科与口腔外科

CiteScore

7.60

自引率

5.30%

发文量

325

审稿时长

4-8 weeks

期刊介绍： Oral Diseases is a multidisciplinary and international journal with a focus on head and neck disorders, edited by leaders in the field, Professor Giovanni Lodi (Editor-in-Chief, Milan, Italy), Professor Stefano Petti (Deputy Editor, Rome, Italy) and Associate Professor Gulshan Sunavala-Dossabhoy (Deputy Editor, Shreveport, LA, USA). The journal is pre-eminent in oral medicine. Oral Diseases specifically strives to link often-isolated areas of dentistry and medicine through broad-based scholarship that includes well-designed and controlled clinical research, analytical epidemiology, and the translation of basic science in pre-clinical studies. The journal typically publishes articles relevant to many related medical specialties including especially dermatology, gastroenterology, hematology, immunology, infectious diseases, neuropsychiatry, oncology and otolaryngology. The essential requirement is that all submitted research is hypothesis-driven, with significant positive and negative results both welcomed. Equal publication emphasis is placed on etiology, pathogenesis, diagnosis, prevention and treatment.