Molecular Mechanism of TRIM16 Regulating Osteogenic Differentiation of Periodontal Ligament Stem Cells Under Inflammatory Microenvironment

IF 3.5 3区生物学 Q3 CELL BIOLOGY

Cell Biology International Pub Date : 2026-08-06 DOI:10.1002/cbin.70192

Xudong Ma

{"title":"Molecular Mechanism of TRIM16 Regulating Osteogenic Differentiation of Periodontal Ligament Stem Cells Under Inflammatory Microenvironment","authors":"Xudong Ma","doi":"10.1002/cbin.70192","DOIUrl":null,"url":null,"abstract":"<div>\n \n <p>This study explores the mechanism of TRIM16 on osteogenic differentiation of human periodontal ligament stem cells (hPDLSCs) in an inflammatory microenvironment. hPDLSCs were cultured and identified by flow cytometry and osteogenesis/adipogenesis induction. hPDLSCs were maintained with <i>P. gingivalis</i> LPS and induced by osteogenic differentiation. TRIM16, HOXA10, and KLF5 expression was tested via RT-qPCR and Western blot. After overexpression of TRIM16, TNF-α, IL-6, and IL-1β levels were examined via ELISA. Osteogenic differentiation of hPDLSCs was validated by Alizarin red staining, ALP staining, and Western blot. The binding of TRIM16 to HOXA10 was detected by Co-IP, and the ubiquitinated HOXA10-containing complexes were measured. Dual luciferase assay and ChIP analyzed the enrichment of HOXA10 on the KLF5 promoter. LPS treatment reduces TRIM16 and KLF5 expression, while elevating HOXA10 protein level. Overexpression of TRIM16 alleviates inflammation in LPS-induced hPDLSCs and enhances osteogenic differentiation. Mechanistically, TRIM16 inhibits HOXA10 protein level via ubiquitination, thereby abating the enrichment of HOXA10 on the KLF5 promoter and promoting the expression of KLF5. In conclusion, TRIM16 facilitates osteogenic differentiation of hPDLSCs in an inflammatory microenvironment via HOXA10/KLF5 axis.</p>\n </div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 8","pages":""},"PeriodicalIF":3.5000,"publicationDate":"2026-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cell Biology International","FirstCategoryId":"99","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/cbin.70192","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CELL BIOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

This study explores the mechanism of TRIM16 on osteogenic differentiation of human periodontal ligament stem cells (hPDLSCs) in an inflammatory microenvironment. hPDLSCs were cultured and identified by flow cytometry and osteogenesis/adipogenesis induction. hPDLSCs were maintained with P. gingivalis LPS and induced by osteogenic differentiation. TRIM16, HOXA10, and KLF5 expression was tested via RT-qPCR and Western blot. After overexpression of TRIM16, TNF-α, IL-6, and IL-1β levels were examined via ELISA. Osteogenic differentiation of hPDLSCs was validated by Alizarin red staining, ALP staining, and Western blot. The binding of TRIM16 to HOXA10 was detected by Co-IP, and the ubiquitinated HOXA10-containing complexes were measured. Dual luciferase assay and ChIP analyzed the enrichment of HOXA10 on the KLF5 promoter. LPS treatment reduces TRIM16 and KLF5 expression, while elevating HOXA10 protein level. Overexpression of TRIM16 alleviates inflammation in LPS-induced hPDLSCs and enhances osteogenic differentiation. Mechanistically, TRIM16 inhibits HOXA10 protein level via ubiquitination, thereby abating the enrichment of HOXA10 on the KLF5 promoter and promoting the expression of KLF5. In conclusion, TRIM16 facilitates osteogenic differentiation of hPDLSCs in an inflammatory microenvironment via HOXA10/KLF5 axis.

查看原文本刊更多论文

炎症微环境下TRIM16调控牙周韧带干细胞成骨分化的分子机制

本研究探讨了TRIM16在炎症微环境下影响人牙周韧带干细胞成骨分化的机制。培养hPDLSCs并通过流式细胞术和成骨/脂肪诱导鉴定。用牙龈卟啉卟啉脂多糖维持hPDLSCs，并通过成骨分化诱导。RT-qPCR和Western blot检测TRIM16、HOXA10、KLF5的表达。过表达TRIM16后，ELISA检测TNF-α、IL-6、IL-1β水平。茜素红染色、ALP染色和Western blot验证hPDLSCs的成骨分化。通过Co-IP检测TRIM16与HOXA10的结合，并测定含HOXA10泛素化复合物。双荧光素酶法和ChIP分析了HOXA10在KLF5启动子上的富集。LPS处理降低TRIM16和KLF5的表达，同时升高HOXA10蛋白水平。TRIM16过表达可减轻脂多糖诱导的hPDLSCs的炎症，增强成骨分化。机制上，TRIM16通过泛素化抑制HOXA10蛋白水平，从而减弱HOXA10在KLF5启动子上的富集，促进KLF5的表达。综上所述，TRIM16通过HOXA10/KLF5轴促进炎症微环境下hPDLSCs的成骨分化。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Cell Biology International 生物-细胞生物学

CiteScore

7.60

自引率

0.00%

发文量

208

审稿时长

1 months

期刊介绍： Each month, the journal publishes easy-to-assimilate, up-to-the minute reports of experimental findings by researchers using a wide range of the latest techniques. Promoting the aims of cell biologists worldwide, papers reporting on structure and function - especially where they relate to the physiology of the whole cell - are strongly encouraged. Molecular biology is welcome, as long as articles report findings that are seen in the wider context of cell biology. In covering all areas of the cell, the journal is both appealing and accessible to a broad audience. Authors whose papers do not appeal to cell biologists in general because their topic is too specialized (e.g. infectious microbes, protozoology) are recommended to send them to more relevant journals. Papers reporting whole animal studies or work more suited to a medical journal, e.g. histopathological studies or clinical immunology, are unlikely to be accepted, unless they are fully focused on some important cellular aspect. These last remarks extend particularly to papers on cancer. Unless firmly based on some deeper cellular or molecular biological principle, papers that are highly specialized in this field, with limited appeal to cell biologists at large, should be directed towards journals devoted to cancer, there being very many from which to choose.