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类风湿关节炎患者外周血单个核细胞中组蛋白去乙酰化酶 3 活性降低和组蛋白 H3 乙酰化增加。

Reduced Activity of HDAC3 and Increased Acetylation of Histones H3 in Peripheral Blood Mononuclear Cells of Patients with Rheumatoid Arthritis.

机构信息

Department of Rheumatology, The First Affiliated Hospital of Xiamen University, Xiamen, Fujian 361003, China.

The First People's Hospital of Yueyang, No. 39, Dongmaoling Road, Yueyang, Hunan 414000, China.

出版信息

J Immunol Res. 2018 Oct 3;2018:7313515. doi: 10.1155/2018/7313515. eCollection 2018.

DOI:10.1155/2018/7313515
PMID:30402512
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6192092/
Abstract

Aberrant histone acetylation and deacetylation are increasingly thought to play important roles in the pathogenesis of rheumatoid arthritis (RA). However, limited data from studies about the activity of histone deacetylases (HDACs) and histone acetyltransferase (HAT) in RA are controversial. Those conflicting results may be caused by sample size, medication, and age- and sex-matched controls. The aim of this study is to investigate the expression and activity of class I HDACs (1-3.8) and their effects on histone acetylation in peripheral blood mononuclear cells (PBMCs) from RA patients. The expression of class I HDACs in PBMCs from RA patients was decreased in both mRNA and protein levels in comparison with HCs. The nuclear HAT activities were dramatically increased. Further, we found HDAC3 activity to be the most significantly reduced in overall reduction of HDACs in the RA group. The extent of total histone H3, but not H4, acetylation in PBMCs from RA patients was increased compared to that in healthy controls (HCs) ( < 0.01). In RA PBMCs, the activity and expression of class I HDACs are decreased, which is accompanied with enhanced HAT activity. An altered balance between HDAC and HAT activity was found in RA PBMCs.

摘要

组蛋白乙酰化和去乙酰化的异常被认为在类风湿关节炎（RA）的发病机制中起着重要作用。然而，关于 RA 中组蛋白去乙酰化酶（HDACs）和组蛋白乙酰转移酶（HAT）活性的研究数据有限，且存在争议。这些相互矛盾的结果可能是由于样本量、药物、年龄和性别匹配的对照组不同所致。本研究旨在探讨 RA 患者外周血单个核细胞（PBMCs）中 I 类 HDAC（1-3.8）的表达和活性及其对组蛋白乙酰化的影响。与健康对照（HC）相比，RA 患者 PBMCs 中 I 类 HDAC 的 mRNA 和蛋白水平表达均降低。核 HAT 活性显著增加。此外，我们发现 RA 组中 HDAC3 活性的降低幅度最大。与健康对照组（HCs）相比，RA 患者 PBMCs 中总组蛋白 H3 的乙酰化程度增加，但 H4 组蛋白的乙酰化程度没有增加（<0.01）。在 RA PBMCs 中，I 类 HDAC 的活性和表达降低，同时 HAT 活性增强。在 RA PBMCs 中发现 HDAC 和 HAT 活性之间的平衡发生改变。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2228/6192092/172921575c91/JIR2018-7313515.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2228/6192092/cf7128b158eb/JIR2018-7313515.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2228/6192092/2e3e92f362ff/JIR2018-7313515.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2228/6192092/6b23c6461283/JIR2018-7313515.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2228/6192092/90c9a087f335/JIR2018-7313515.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2228/6192092/6b7e8af8e971/JIR2018-7313515.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2228/6192092/5e44e2519361/JIR2018-7313515.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2228/6192092/ae96c28d73df/JIR2018-7313515.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2228/6192092/172921575c91/JIR2018-7313515.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2228/6192092/cf7128b158eb/JIR2018-7313515.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2228/6192092/2e3e92f362ff/JIR2018-7313515.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2228/6192092/6b23c6461283/JIR2018-7313515.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2228/6192092/90c9a087f335/JIR2018-7313515.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2228/6192092/6b7e8af8e971/JIR2018-7313515.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2228/6192092/5e44e2519361/JIR2018-7313515.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2228/6192092/ae96c28d73df/JIR2018-7313515.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2228/6192092/172921575c91/JIR2018-7313515.008.jpg

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本文引用的文献

[1]
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Aberrant histone acetylation contributes to elevated interleukin-6 production in rheumatoid arthritis synovial fibroblasts.

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Imbalance between HAT and HDAC activities in the PBMCs of patients with ankylosing spondylitis or rheumatoid arthritis and influence of HDAC inhibitors on TNF alpha production.

PLoS One. 2013-8-15

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Arthritis Rheum. 2013-7

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