六磷酸肌醇(InsP6)激活 HDAC1/3 表观遗传轴以维持肠道屏障功能

Sujan Chatterjee, Loretta Viera Preval, Zachary Sin, Nguyen Tran, Kevin Ritter, Xue Bessie Su, Jakob P. Centlivre, Saharat Jolak Ragsac, Richard Van, Seungman Park, Mira Han, Qian Liu, Brian P Hedlund, Adolfo Saiardi, Henning Jessen, Dr Prasun Guha
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引用次数: 0

摘要

HDAC(组蛋白去乙酰化酶)在调节基因表达方面起着至关重要的作用,而抑制这些酶作为一种有前途的癌症治疗方法正日益受到关注。尽管HDAC具有重要的生理和临床意义,但人们对其激活机制仍然知之甚少。本研究揭示了肌醇多磷酸多激酶(IPMK)对于激活细胞系和小鼠中的 HDAC1 和 HDAC3 至关重要。IPMK 缺失或其激酶活性失活会选择性地损害 HDAC1/3 的去乙酰化酶活性,从而显著影响基因表达。IPMK-HDAC1/3 表观遗传轴的破坏会导致基质金属蛋白酶(MMP)基因的转录上调,从而加剧细胞和肠道的通透性。值得注意的是,用具有细胞渗透性的六磷酸肌醇(InsP6)处理 IPMK KO 细胞可挽救这些缺陷。这项研究阐明了 IPMK 激酶活性在 HDAC1/3 激活中的作用及其对肠道屏障功能的影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Inositol Hexaphosphate (InsP6) Activates the HDAC1/3 Epigenetic Axis to Maintain Intestinal Barrier Function
HDACs (histone deacetylase) play a crucial role in regulating gene expression, and the inhibition of these enzymes is gaining attention as a promising therapeutic approach for cancer treatment. Despite their significant physiological and clinical importance, the mechanisms of HDAC activation remain poorly understood. This study reveals that inositol polyphosphate multikinase (IPMK) is essential for activating HDAC1 and HDAC3 in cell lines and mice. IPMK deletion or inactivation of its kinase activity selectively impairs HDAC1/3's deacetylase activity, significantly influencing gene expression. Disruption of the IPMK-HDAC1/3 epigenetic axis results in transcriptional upregulation of matrix metalloproteinase (MMP) genes, exacerbating cell and intestinal permeability. Remarkably, treatment of IPMK KO cells with cell-permeable inositol hexaphosphate (InsP6) rescues these defects. This study elucidates the role of IPMK's kinase activity in HDAC1/3 activation and its implications for intestinal barrier function.
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