Cell Death Differ:RNF20和RNF40是炎症性肠病的关键调节因子

2021-06-06 xiaozeng MedSci原创

炎症性肠病(IBD),包括克罗恩病(CD)和溃疡性结肠炎(UC),在欧洲和北美人里约每250名有一人受该疾病影响。

炎症性肠病(IBD),包括克罗恩病(CD)和溃疡性结肠炎(UC),在欧洲和北美人里约每250名有一人受该疾病影响。人群中IBD发病率的快速增加也提示与疾病易感性相关的环境因素。而环境暴露与病理生理学之间的一大主要联系性为染色质修饰可稳定改变转录程序和细胞功能。

尽管目前已确定了与炎症性肠病(IBD)易感性增加的几种相关遗传因素,但其潜在的分子机制仍有待进一步的阐明。研究人员发现,泛素连接酶RNF20和RNF40能够介导组蛋白H2B第120位赖氨酸的单泛素化(H2Bub1),且显示出其在炎症发生发展过程中起承上启下的作用。

该研究旨在探究RNF20/RNF40/H2Bub1通路在IBD患者和肠道炎症小鼠模型中的功能。研究人员通过对IBD患者的肠道切片进行了H2Bub1的免疫组化染色,在小鼠肠道中条件性的敲除Rnf20或Rnf40并监测小鼠的炎症相关症状。

IBD患者的炎症性肠上皮中H2Bub1的水平降低

研究人员发现,大多数(80%)IBD患者的发炎区域中H2Bub1的水平降低,且条件性敲除小鼠会出现自发性结直肠炎症的发生。同样的,敲除Rnf20或Rnf40会促进IBD相关基因的表达,包括各种IBD风险基因的失调。

条件性敲除Rnf20和Rnf40会导致自发性结直肠炎症的发生

对小鼠的原代肠上皮细胞(IEC)的进一步分析显示,Vdr(维生素D受体)基因和VDR靶基因的H3K4me3状态和转录均依赖于RNF20/40。上述的这些影响在克罗恩病患者亚组中也同样得到证实,这些患者在RNF20/40依赖性的基因表征中呈现出了表观遗传和基因表达上的改变。


总而言之,该研究结果表明,H2B单泛素化的缺失可通过降低VDR的活性并促进肠道炎症的发生,而RNF20和RNF40是IBD的关键调节因子。


原始出处:

Kosinsky, R.L., Zerche, M., Kutschat, A.P. et al. RNF20 and RNF40 regulate vitamin D receptor-dependent signaling in inflammatory bowel disease. Cell Death Differ (04 June 2021).

 

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    2022-01-11 维他命
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    2021-07-29 isabellayj
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    2021-06-08 cy0328
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    2021-06-06 smart Ren

    认真学习

    0

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    2021-06-06 医鸣惊人

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