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suppresses post-ischemic natural killer cell infiltration and activation in the brain: involvement of histonedeacetylase inhibition

Baokai Dou, Shichun Li, Luyao Wei, Lixin Wang, Shiguo Zhu, Zhengtao Wang, Zunji Ke, Kaixian Chen, Zhifei Wang

《医学前沿（英文）》 2021年 第15卷 第1期   页码 79-90 doi: 10.1007/s11684-020-0783-8

摘要： Natural killer (NK) cells, a type of cytotoxic lymphocytes, can infiltrate into ischemic brain and exacerbate neuronal cell death. Astragaloside IV (ASIV) is the major bioactive ingredient of , a Chinese herbal medicine, and possesses potent immunomodulatory and neuroprotective properties. This study investigated the effects of ASIV on post-ischemic brain infiltration and activation of NK cells. ASIV reduced brain infarction and alleviated functional deficits in MCAO rats, and these beneficial effects persisted for at least 7 days. Abundant NK cells infiltrated into the ischemic hemisphere on day 1 after brain ischemia, and this infiltration was suppressed by ASIV. Strikingly, ASIV reversed NK cell deficiency in the spleen and blood after brain ischemia. ASIV inhibited astrocyte-derived CCL2 upregulation and reduced CCR2 NK cell levels in the ischemic brain. Meanwhile, ASIV attenuated NK cell activating receptor NKG2D levels and reduced interferon-γ production. ASIV restored acetylation of histone H3 and the p65 subunit of nuclear factor-κB in the ischemic brain, suggesting inhibition of histone deacetylase (HDAC). Simultaneously, ASIV prevented p65 nuclear translocation. The effects of ASIV on reducing CCL2 production, restoring acetylated p65 levels and preventing p65 nuclear translocation were mimicked by valproate, an HDAC inhibitor, in astrocytes subjected to oxygen-glucose deprivation. Our findings suggest that ASIV inhibits post-ischemic NK cell brain infiltration and activation and reverses NK cell deficiency in the periphery, which together contribute to the beneficial effects of ASIV against brain ischemia. Furthermore, ASIV’s effects on suppressing NK cell brain infiltration and activation may involve HDAC inhibition.

关键词： astragaloside IV     brain ischemia     natural killer cells     histone deacetylase     nuclear factor-κB    

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Effects of hydralazine and valproate on the expression of E-cadherin gene and the invasiveness of QBC

Hong LI, Shaoqin CHEN, Yi SHU, Yongjun CHEN, Ying SU, Xin WANG, Shengquan ZOU

《医学前沿（英文）》 2009年 第3卷 第2期   页码 153-157 doi: 10.1007/s11684-009-0034-5

摘要： To clarify the effect of DNA methylation and histone deacetylase inhibitors on the expression of the E-cadherin gene and the invasiveness of the QBC cells, the QBC cells were separately treated with hydralazine, valproate, or combination of the two drugs. The mRNA expression of E-cadherin was examined with reverse transcription-polymerase chain reaction (RT-PCR), the protein of the gene with Western blotting. The methylation status of the promoter region of the gene was detected with methylation-specific PCR (MSP). The invasiveness of QBC cells was detected with transwell assay. It was found that the promoter region of the E-cadherin gene of QBC cells was hypermethylated. Valproate alone could not contribute to demethylation of the gene, whereas hydralazine could make them to be partly demethylated. However, the methylation status of the gene could be thoroughly reversed by using valproate and hydralazine in combination. What’s more, it was confirmed that the E-cadherin gene of QBC cells could not be transcriptionally reactivated by Valproate alone, whereas hydralazine alone could induce moderate reexpression of the gene. However, using valproate and hydralazine in combination could result in robust reexpression of the E-cadherin gene ( =0.000). Likewise, the invasiveness of the QBC939 cells was sharply decreased by treatment with two drugs in combination and slightly decreased with one drug alone. It could be concluded that the two drugs have synergistic effect on the demethylation and reexpression of the E-cadherin gene of QBC cells, and also on the reduction of the invasiveness of the QBC939 cells.

关键词： DNA methylation inhibitor     histone deacetylase inhibitor     bile duct carcinoma     E-cadherin    

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Regulation and function of histone acetyltransferase MOF

null

《医学前沿（英文）》 2014年 第8卷 第1期   页码 79-83 doi: 10.1007/s11684-014-0314-6

摘要：

The mammalian MOF (male absent on the first), a member of the MYST (MOZ, YBF2, SAS2, and Tip60) family of histone acetyltransferases (HATs), is the major enzyme that catalyzes the acetylation of histone H4 on lysine 16. Acetylation of K16 is a prevalent mark associated with chromatin decondensation. MOF has recently been shown to play an essential role in maintaining normal cell functions. In this study, we discuss the important roles of MOF in DNA damage repair, apoptosis, and tumorigenesis. We also analyze the role of MOF as a key regulator of the core transcriptional network of embryonic stem cells.

关键词： MOF     histone acetyltransferase     DNA damage repair     tumorigenesis     embryonic stem cells    

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The secondary laticifer differentiation in rubber tree is induced by trichostatin A, an inhibitor of histone

Shixin ZHANG,Shaohua WU,Weimin TIAN

《农业科学与工程前沿（英文）》 2016年 第3卷 第4期   页码 357-362 doi: 10.15302/J-FASE-2016125

摘要： The secondary laticifer, a specific tissue in the secondary phloem of rubber tree, is differentiated from the vascular cambia. The number of the secondary laticifer in the trunk bark of rubber tree is positively correlated with rubber yield. Although jasmonates have been demonstrated to be crucial in the regulation of secondary laticifer differentiation, the mechanism for the jasmonate-induced secondary laticifer differentiation remains to be elucidated. By using an experimental morphological technique, the present study revealed that trichostatin A (TSA), an inhibitor of histone deacetylation, could induce the secondary laticifer differentiation in a concentration-dependent manner. The results suggest that histone acetylation is essential for the secondary laticifer differentiation in rubber tree.

关键词： Hevea brasiliensis     histone acetylation     laticifer differentiation     trichostatin     vascular cambia    

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The critical importance of epigenetics in autoimmune-related skin diseases

《医学前沿（英文）》 2023年 第17卷 第1期   页码 43-57 doi: 10.1007/s11684-022-0980-8

摘要： Autoimmune-related skin diseases are a group of disorders with diverse etiology and pathophysiology involved in autoimmunity. Genetics and environmental factors may contribute to the development of these autoimmune disorders. Although the etiology and pathogenesis of these disorders are poorly understood, environmental variables that induce aberrant epigenetic regulations may provide some insights. Epigenetics is the study of heritable mechanisms that regulate gene expression without changing DNA sequences. The most important epigenetic mechanisms are DNA methylation, histone modification, and noncoding RNAs. In this review, we discuss the most recent findings regarding the function of epigenetic mechanisms in autoimmune-related skin disorders, including systemic lupus erythematosus, bullous skin diseases, psoriasis, and systemic sclerosis. These findings will expand our understanding and highlight the possible clinical applications of precision epigenetics approaches.

关键词： epigenetics     autoimmune-related skin diseases     DNA methylation     histone modifications     noncoding RNAs    

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Epigenetic dysregulation in hepatocellular carcinoma: focus on polycomb group proteins

null

《医学前沿（英文）》 2013年 第7卷 第2期   页码 231-241 doi: 10.1007/s11684-013-0253-7

摘要：

Hepatocellular carcinoma (HCC) development is characterized by the presence of epigenetic alterations, including promoter DNA hypermethylation and post-translational modifications of histone, which profoundly affect expression of a wide repertoire of genes critical for cancer development. Emerging data suggest that deregulation of polycomb group (PcG) proteins, which are key chromatin modifiers repressing gene transcription during developmental stage, plays a causative role in oncogenesis. PcG proteins assemble into polycomb repressive complex 1 (PRC1) and polycomb repressive complex 2 (PRC2) to impose the histone H3 lysine 27 trimethylation (H3K27me3) modification for repression. In this review, we will first recapitulate the mechanisms of two key epigenetic pathways: DNA methylation and histone modifications. Specifically, we will focus our discussion on the molecular roles of PcG proteins. Next, we will highlight recent findings on PcG proteins, their clinicopathological implication and their downstream molecular consequence in hepatocarcinogenesis. Last but not least, we will consider the therapeutic potential of targeting enhancer of zeste homolog 2 (EZH2) as a possible treatment for HCC. Improving our understanding on the roles of PcG proteins in hepatocarcinogenesis can benefit the development of epigenetic-based therapy.

关键词： liver cancer     epigenetics     histone modifications     polycomb group proteins     enhancer of zeste homolog 2 (EZH2)    

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Histone variants: critical determinants in tumour heterogeneity

Tao Wang, Florent Chuffart, Ekaterina Bourova-Flin, Jin Wang, Jianqing Mi, Sophie Rousseaux, Saadi Khochbin

《医学前沿（英文）》 2019年 第13卷 第3期   页码 289-297 doi: 10.1007/s11684-018-0667-3

摘要： Malignant cell transformation could be considered as a series of cell reprogramming events driven by oncogenic transcription factors and upstream signalling pathways. Chromatin plasticity and dynamics are critical determinants in the control of cell reprograming. An increase in chromatin dynamics could therefore constitute an essential step in driving oncogenesis and in generating tumour cell heterogeneity, which is indispensable for the selection of aggressive properties, including the ability of cells to disseminate and acquire resistance to treatments. Histone supply and dosage, as well as histone variants, are the best-known regulators of chromatin dynamics. By facilitating cell reprogramming, histone under-dosage and histone variants should also be crucial in cell transformation and tumour metastasis. Here we summarize and discuss our knowledge of the role of histone supply and histone variants in chromatin dynamics and their ability to enhance oncogenic cell reprogramming and tumour heterogeneity.

关键词： cancer-testis     TH2B     TH2A     H1T     H1.0     H1F0     linker histones    

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标题 作者 时间 类型 操作

suppresses post-ischemic natural killer cell infiltration and activation in the brain: involvement of histonedeacetylase inhibition

Baokai Dou, Shichun Li, Luyao Wei, Lixin Wang, Shiguo Zhu, Zhengtao Wang, Zunji Ke, Kaixian Chen, Zhifei Wang

期刊论文

Effects of hydralazine and valproate on the expression of E-cadherin gene and the invasiveness of QBC

Hong LI, Shaoqin CHEN, Yi SHU, Yongjun CHEN, Ying SU, Xin WANG, Shengquan ZOU

期刊论文

Regulation and function of histone acetyltransferase MOF

null

期刊论文

The secondary laticifer differentiation in rubber tree is induced by trichostatin A, an inhibitor of histone

Shixin ZHANG,Shaohua WU,Weimin TIAN

期刊论文

The critical importance of epigenetics in autoimmune-related skin diseases

期刊论文

Epigenetic dysregulation in hepatocellular carcinoma: focus on polycomb group proteins

null

期刊论文

Histone variants: critical determinants in tumour heterogeneity

Tao Wang, Florent Chuffart, Ekaterina Bourova-Flin, Jin Wang, Jianqing Mi, Sophie Rousseaux, Saadi Khochbin

期刊论文