Role of transglutaminase 2 in promoting biglycan synthesis in idiopathic gingival fibromatosis.

IF 2.6 2区医学 Q1 DENTISTRY, ORAL SURGERY & MEDICINE

BMC Oral Health Pub Date : 2024-11-21 DOI:10.1186/s12903-024-05211-8

Yurika Ninomiya, Shinji Matsuda, Shigeki Suzuki, Shizu Hirata-Tsuchiya, Tomoya Ueda, Fuminori Nakashima, Keisuke Yasuda, Shogo Shimada, Takumi Memida, Tetsuya Yoshimoto, Satoru Yamada, Kazuhisa Ouhara, Noriyoshi Mizuno

{"title":"Role of transglutaminase 2 in promoting biglycan synthesis in idiopathic gingival fibromatosis.","authors":"Yurika Ninomiya, Shinji Matsuda, Shigeki Suzuki, Shizu Hirata-Tsuchiya, Tomoya Ueda, Fuminori Nakashima, Keisuke Yasuda, Shogo Shimada, Takumi Memida, Tetsuya Yoshimoto, Satoru Yamada, Kazuhisa Ouhara, Noriyoshi Mizuno","doi":"10.1186/s12903-024-05211-8","DOIUrl":null,"url":null,"abstract":"Background: This study aimed to elucidate the pathogenesis of idiopathic gingival fibromatosis (IGF).Methods: Human gingival fibroblasts (hGFs) were isolated from patients with IGF and periodontitis. Differential gene expression in the hGFs was analyzed using RNA sequencing. Extracellular matrix-related gene expression in the hGFs was analyzed. The effect of specific protein (SP)1 inhibitor or recombinant human transglutaminase 2 (rh-TGM2) on biglycan (BGN) expression in hGFs was also determined.Results: RNA sequencing showed that TGM2 expression was downregulated and BGN mRNA expression was upregulated in patients with IGF relative to periodontitis. rh-TGM2 stimulation of hGFs in patients with IGF significantly reduced BGN expression. SP1 inhibitors downregulated BGN expression in the hGFs.Conclusion: BGN upregulation via SP1 causes TGM2 downregulation in gingival fibroblasts in IGF.","PeriodicalId":9072,"journal":{"name":"BMC Oral Health","volume":"24 1","pages":"1422"},"PeriodicalIF":2.6000,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"BMC Oral Health","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1186/s12903-024-05211-8","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"DENTISTRY, ORAL SURGERY & MEDICINE","Score":null,"Total":0}

引用次数: 0

Abstract

Background: This study aimed to elucidate the pathogenesis of idiopathic gingival fibromatosis (IGF).

Methods: Human gingival fibroblasts (hGFs) were isolated from patients with IGF and periodontitis. Differential gene expression in the hGFs was analyzed using RNA sequencing. Extracellular matrix-related gene expression in the hGFs was analyzed. The effect of specific protein (SP)1 inhibitor or recombinant human transglutaminase 2 (rh-TGM2) on biglycan (BGN) expression in hGFs was also determined.

Results: RNA sequencing showed that TGM2 expression was downregulated and BGN mRNA expression was upregulated in patients with IGF relative to periodontitis. rh-TGM2 stimulation of hGFs in patients with IGF significantly reduced BGN expression. SP1 inhibitors downregulated BGN expression in the hGFs.

Conclusion: BGN upregulation via SP1 causes TGM2 downregulation in gingival fibroblasts in IGF.

查看原文本刊更多论文

转谷氨酰胺酶 2 在特发性牙龈纤维瘤病中促进大聚糖合成的作用

背景：本研究旨在阐明特发性牙龈纤维瘤病（IGF）的发病机制：方法：从特发性牙龈纤维瘤（IGF）和牙周炎患者体内分离出人牙龈成纤维细胞（hGFs）。方法：从 IGF 和牙周炎患者体内分离出人牙龈成纤维细胞（hGFs），利用 RNA 测序分析了 hGFs 中不同基因的表达情况。分析了 hGFs 中细胞外基质相关基因的表达。此外，还测定了特异性蛋白（SP）1抑制剂或重组人转谷氨酰胺酶2（rh-TGM2）对hGFs中biglycan（BGN）表达的影响：RNA测序显示，相对于牙周炎，IGF患者的TGM2表达下调，BGN mRNA表达上调。SP1抑制剂下调了hGFs中BGN的表达：结论：通过 SP1 上调 BGN 会导致 IGF 患者牙龈成纤维细胞中的 TGM2 下调。

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

BMC Oral Health DENTISTRY, ORAL SURGERY & MEDICINE-

CiteScore

3.90

自引率

6.90%

发文量

481

审稿时长

6-12 weeks

期刊介绍： BMC Oral Health is an open access, peer-reviewed journal that considers articles on all aspects of the prevention, diagnosis and management of disorders of the mouth, teeth and gums, as well as related molecular genetics, pathophysiology, and epidemiology.