Scholarlink

Abstract <p>Over recent decades, the prevalence of inflammatory boweldiseases (IBD) has increased worldwide. Following industrialization,the rise in IBD incidence is observed not only in Europe and NorthAmerica but also in Asian countries, including China and India.Despite its widespread occurrence and extensive research, the causesof IBD remain incompletely understood. Epigenetic mechanisms, suchas DNA methylation and post-translational histone modifications,play an important role in IBD pathogenesis. Histone modificationsdetermine chromatin structure and can serve as markers for bothtranscriptionally active and inactive regions. Given the globalalterations in the intestinal gene expression profile in IBD patients,it can be assumed that the development of inflammatory processes(colitis) in the intestine is accompanied by comprehensive structuralalterations in chromatin activity and accessibility at the level ofboth mucosal immune cells and epithelial cells. Specifically, studiesusing intestinal tissue samples from patients with enterocolitishave shown a decrease in the total amount of histone H3 lysine 27 trimethylation(H3K27me3) in epithelial cells. Simultaneously, inhibition of H3K27trimethylation is a promising approach to IBD treatment throughtranscription regulation in immune cells. This work investigatedthe abundance of this histone modification in the nuclei of epithelialcells and in the colonic tissue as a whole in two mouse models ofchronic colitis. It was shown that the overall H3K27me3 level increasesin the nuclei of enterocytes in the murine <i>Muc2</i> geneknockout model of chronic colitis. This result suggests a significantimpact of the H3K27me3 modification on the pathogenesis of IBD notonly in immune but also in colonic epithelial cells.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

The Abundance of H3K27me3 Histone Modification in the Mouse Colon under Chronic Inflammation

  • 期刊论文

  • 发表日期：

    2025年7月1日

查看全文
  • E. A. Nickelwart,
  • S. S. Medvedeva,
  • J. V. Popova,
  • E. N. Kozhevnikova

摘要

Abstract

Over recent decades, the prevalence of inflammatory boweldiseases (IBD) has increased worldwide. Following industrialization,the rise in IBD incidence is observed not only in Europe and NorthAmerica but also in Asian countries, including China and India.Despite its widespread occurrence and extensive research, the causesof IBD remain incompletely understood. Epigenetic mechanisms, suchas DNA methylation and post-translational histone modifications,play an important role in IBD pathogenesis. Histone modificationsdetermine chromatin structure and can serve as markers for bothtranscriptionally active and inactive regions. Given the globalalterations in the intestinal gene expression profile in IBD patients,it can be assumed that the development of inflammatory processes(colitis) in the intestine is accompanied by comprehensive structuralalterations in chromatin activity and accessibility at the level ofboth mucosal immune cells and epithelial cells. Specifically, studiesusing intestinal tissue samples from patients with enterocolitishave shown a decrease in the total amount of histone H3 lysine 27 trimethylation(H3K27me3) in epithelial cells. Simultaneously, inhibition of H3K27trimethylation is a promising approach to IBD treatment throughtranscription regulation in immune cells. This work investigatedthe abundance of this histone modification in the nuclei of epithelialcells and in the colonic tissue as a whole in two mouse models ofchronic colitis. It was shown that the overall H3K27me3 level increasesin the nuclei of enterocytes in the murine Muc2 geneknockout model of chronic colitis. This result suggests a significantimpact of the H3K27me3 modification on the pathogenesis of IBD notonly in immune but also in colonic epithelial cells.