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Dynamic alterations of H3K4me3 and H3K27me3 at ADAM17 and Jagged‐1 gene promoters cause an inflammatory switch of endothelial cells

H3K4me3 组蛋白H3 组蛋白甲基转移酶 生物 表观遗传学 EZH2型 组蛋白甲基化 组蛋白 细胞生物学 炎症 癌症研究 DNA甲基化 基因表达 发起人 免疫学 遗传学 基因
作者
Yash T. Katakia,Niyati Pandya Thakkar,Sumukh Thakar,Ashima Sakhuja,Raghav Goyal,Harshita Sharma,Rakshita Dave,Ayushi Mandloi,Sayan Basu,Ishan Nigam,Bhanu Vardhan Reddy Kuncharam,Shibasish Chowdhury,Syamantak Majumder
出处
期刊:Journal of Cellular Physiology [Wiley]
卷期号:237 (1): 992-1012 被引量:12
标识
DOI:10.1002/jcp.30579
摘要

Histone protein modifications control the inflammatory state of many immune cells. However, how dynamic alteration in histone methylation causes endothelial inflammation and apoptosis is not clearly understood. To examine this, we explored two contrasting histone methylations; an activating histone H3 lysine 4 trimethylation (H3K4me3) and a repressive histone H3 lysine 27 trimethylation (H3K27me3) in endothelial cells (EC) undergoing inflammation. Through computer-aided reconstruction and 3D printing of the human coronary artery, we developed a unique model where EC were exposed to a pattern of oscillatory/disturbed flow as similar to in vivo conditions. Upon induction of endothelial inflammation, we detected a significant rise in H3K4me3 caused by an increase in the expression of SET1/COMPASS family of H3K4 methyltransferases, including MLL1, MLL2, and SET1B. In contrast, EC undergoing inflammation exhibited truncated H3K27me3 level engendered by EZH2 cytosolic translocation through threonine 367 phosphorylation and an increase in the expression of histone demethylating enzyme JMJD3 and UTX. Additionally, many SET1/COMPASS family of proteins, including MLL1 (C), MLL2, and WDR5, were associated with either UTX or JMJD3 or both and such association was elevated in EC upon exposure to inflammatory stimuli. Dynamic enrichment of H3K4me3 and loss of H3K27me3 at Notch-associated gene promoters caused ADAM17 and Jagged-1 derepression and abrupt Notch activation. Conversely, either reducing H3K4me3 or increasing H3K27me3 in EC undergoing inflammation attenuated Notch activation, endothelial inflammation, and apoptosis. Together, these findings indicate that dynamic chromatin modifications may cause an inflammatory and apoptotic switch of EC and that epigenetic reprogramming can potentially improve outcomes in endothelial inflammation-associated cardiovascular diseases.
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