Suppr超能文献

牙龈密螺旋体通过可逆的 DNA 和组蛋白修饰增加牙周组织中 MMP-2 的表达和激活。

Treponema denticola increases MMP-2 expression and activation in the periodontium via reversible DNA and histone modifications.

机构信息

Department of Periodontics and Oral Medicine, University of Michigan School of Dentistry, Ann Arbor, MI, USA.

Department of Periodontics and Oral Medicine, University of Mansoura Faculty of Dentistry, Mansoura, Egypt.

出版信息

Cell Microbiol. 2018 Apr;20(4). doi: 10.1111/cmi.12815. Epub 2018 Jan 8.

Abstract

Host-derived matrix metalloproteinases (MMPs) and bacterial proteases mediate destruction of extracellular matrices and supporting alveolar bone in periodontitis. The Treponema denticola dentilisin protease induces MMP-2 expression and activation in periodontal ligament (PDL) cells, and dentilisin-mediated activation of pro-MMP-2 is required for cellular fibronectin degradation. Here, we report that T. denticola regulates MMP-2 expression through epigenetic modifications in the periodontium. PDL cells were treated with epigenetic enzyme inhibitors before or after T. denticola challenge. Fibronectin fragmentation, MMP-2 expression, and activation were assessed by immunoblot, zymography, and qRT-PCR, respectively. Chromatin modification enzyme expression in T. denticola-challenged PDL cells and periodontal tissues were evaluated using gene arrays. Several classes of epigenetic enzymes showed significant alterations in transcription in diseased tissue and T. denticola-challenged PDL cells. T. denticola-mediated MMP-2 expression and activation were significantly reduced in PDL cells treated with inhibitors of aurora kinases and histone deacetylases. In contrast, DNA methyltransferase inhibitors had little effect, and inhibitors of histone acetyltransferases, methyltransferases, and demethylases exacerbated T. denticola-mediated MMP-2 expression and activation. Chronic epigenetic changes in periodontal tissues mediated by T. denticola or other oral microbes may contribute to the limited success of conventional treatment of chronic periodontitis and may be amenable to therapeutic reversal.

摘要

宿主来源的基质金属蛋白酶 (MMPs) 和细菌蛋白酶介导牙周炎中细胞外基质和支持性牙槽骨的破坏。牙龈卟啉单胞菌的牙龈蛋白酶诱导牙周韧带 (PDL) 细胞中 MMP-2 的表达和激活,并且牙龈蛋白酶介导的 pro-MMP-2 激活是细胞纤维连接蛋白降解所必需的。在这里,我们报告了 T. denticola 通过牙周组织中的表观遗传修饰来调节 MMP-2 的表达。在 T. denticola 挑战之前或之后,用表观遗传酶抑制剂处理 PDL 细胞。通过免疫印迹、酶谱分析和 qRT-PCR 分别评估纤维连接蛋白片段化、MMP-2 表达和激活。使用基因芯片评估 T. denticola 挑战的 PDL 细胞和牙周组织中染色质修饰酶的表达。几种表观遗传酶类在患病组织和 T. denticola 挑战的 PDL 细胞中的转录水平发生了显著改变。在用 Aurora 激酶和组蛋白去乙酰化酶抑制剂处理的 PDL 细胞中,T. denticola 介导的 MMP-2 表达和激活显著降低。相比之下,DNA 甲基转移酶抑制剂的作用很小,而组蛋白乙酰转移酶、甲基转移酶和去甲基酶抑制剂则加剧了 T. denticola 介导的 MMP-2 表达和激活。T. denticola 或其他口腔微生物介导的牙周组织中的慢性表观遗传变化可能导致慢性牙周炎的常规治疗效果有限,并且可能适合治疗逆转。

相似文献

引用本文的文献

10
Periodontal Disease: The Good, The Bad, and The Unknown.牙周病:好的、坏的和未知的。
Front Cell Infect Microbiol. 2021 Dec 7;11:766944. doi: 10.3389/fcimb.2021.766944. eCollection 2021.

本文引用的文献

1
Pathogenic mechanisms of intracellular bacteria.细胞内细菌的致病机制。
Curr Opin Infect Dis. 2017 Jun;30(3):309-315. doi: 10.1097/QCO.0000000000000363.
8
Epigenetic Mechanisms Governing Innate Inflammatory Responses.调控先天性炎症反应的表观遗传机制
J Interferon Cytokine Res. 2016 Jul;36(7):454-61. doi: 10.1089/jir.2016.0003.

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验