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find Keyword "组蛋白" 19 results
  • Research Progress of the Regulation Function of Epigenetics on Bone Marrow Mesenchymal Stem Cells

    The regulation of epigenetics on bone marrow mesenchymal stem cells (BMSCs) has been a research hot spot in medical area. This paper mainly summarizes the progress of the regulation of DNA methylation, histone acetylation, small interfering RNA (siRNA) induced gene silence and microRNA (miRNA) on BMSCs. Our analysis shows that the regulation of epigenetics on BMSCs plays a significant role in the repair of bone tissue, nervous tissue and cardiac muscle.

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  • BIX-01294 inhibits the proliferation of esophageal squamous cell carcinoma cells by inducing DNA damage and activating the mitochondrial apoptosis pathway

    ObjectiveTo explore the effects and molecular mechanisms of histone methylase G9a inhibitor BIX-01294 on apoptosis in esophageal squamous cell carcinoma (ESCC).MethodsMTT assay and Colony-forming Units were adopted to determine the effects of BIX-01294 on the growth and proliferation of ESCC cell lines EC109 and KYSE150. Flow cytometry was used to analyze the apoptosis status of ESCC cells after the treatment of BIX-01294. The effects of BIX-01294 treatment on the expressions of G9a catalytic product H3K9me2, DNA double-strand break (DSB) markers, and apoptosis-related proteins were detected by Western blotting.ResultsBIX-01294 inhibited the growth of EC109 and KYSE150 cells in a dose-dependent manner (P<0.05), and BIX-01294 with the inhibitory concentration 50% (IC50) significantly inhibited the formation of colony (P<0.05). After 24 hours treatment of BIX-01294 (IC50), the apoptosis rate of EC109 cells increased from 11.5%±2.1% to 42.5%±5.4%, and KYSE150 cells from 7.5%±0.9% to 49.2%±5.2% (P<0.05). The expression level of the G9a catalytic product, H3K9me2, significantly decreased (P<0.05); while the expression of the DSB marker γH2AX was dramatically enhanced (P<0.05). We also found that the mitochondrial apoptosis pathway was activated and the expression levels of cleaved caspase3 and cleaved PARP were significantly elevated (P<0.05).ConclusionBIX-01294, the inhibitor of methyltransferase G9a, prompted apoptosis in ESCC cells by inducing DSB damage and activating mitochondrial apoptosis pathway.

    Release date:2021-06-07 02:03 Export PDF Favorites Scan
  • Acetylated Histone Expressions of the Primary Hippocampal Neurons in Rats Reduced by siCBP Lentivirus

    This study aims to construct the recombinant lentivirus vector containing specific small interfering RNA (siRNA) targeting rat CREB binding protein(CBP)gene and to identify its function of inhibiting the expressions of acetylated histone in primarily cultured hippocampal neurons. Firstly, we constructed four kinds of recombinant lentivirus siCBP. And then we used them to infect the primarily cultured hippocampal neurons, and performed real-time PCR, western blot respectively to detect the expressions of CBP. Afterwards, the most effective lentivirus siCBP was used to infect the primarily cultured hippocampal neurons, and then the HAT activity and protein expressions of acetylated histone Ac-H3, Ac-H4 of the neurons were examined. By using PCR, endonuclease cutting and gene sequencing, we confirmed that the target genes were correctly cloned in lentivirus vector. Besides, CBP mRNA and protein expressions in neurons were found to be with varying degrees of decreases after infections of the four kinds of lentivirus siCBP. Furthermore, the representative and most effective lentivirus GR806 could effectively inhibit the HAT activity and the protein expressions of Ac-H3, Ac-H4 in neurons. It provides the experimental basis for the subsequent application of siCBP to clarify the effects and corresponding molecular mechanism of the CBP-dependent histone acetylation on learning and memory function in hippocampus.

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  • 组蛋白去泛素化修饰的研究进展及其与肿瘤的关系

    组蛋白泛素化及去泛素化为两个可逆的过程,在基因转录后修饰以及细胞稳态的调控中起关键作用。组蛋白去泛素化可通过变化组蛋白修饰从而调控各种原癌基因及抑癌基因表达,使其在肿瘤的发生、发展中起重要作用,逐渐成为肿瘤治疗的研究热点。现就组蛋白去泛素化修饰相关内容及其在肿瘤发生发展中扮演的角色加以综述,为肿瘤的早期诊断和基因治疗提供新的途径和思路。

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  • Expression of Histone Deacetylases 1 and It′s Effects on Histone Modifications in T Cells Isolated from Lungs of Asthmatic Wistar Rats

    Objective To investigate the expression of the histone deacetylases 1( HDAC1) and the level of whole histone acetylation and methylation in lung T cells of asthmatic rats, and investigate their role in the pathogenesis of asthma.Methods Sixteen wistar rats were randomly divided into a control group and an asthma group( n =8 in each group) . The rats was sensitized with ovalbumin( OVA) and challenged with aerosol OVA to establish asthma model. The asthmatic ratmodel was confirmed by measurement of pulmonary function, histochemical staining, HE staining, and the levels of interleukin-4 ( IL-4 ) , interferon-gamma ( IFN-γ) and immunoglobulin E( IgE) in serum and bronchoalveolar lavage fluid ( BALF) . T cells were isolated fromrat lungs and the purity was identified. The expression of the HDAC1, the level of whole histone H3 and H4 acetylation, and whole H3K9 dimethylation were analyzed by Western blot in lung T cells. Results Compared with the control group, the protein expression of HDAC1 was significantly lower( 0. 465±0. 087 vs 0. 790 ±0. 076, P lt;0. 05) in lung T cells of the asthma group. No significant differences werefound in regard to the level of whole histone H3 and H4 acetylation and whole H3K9 dimethylation betweenthe two groups. Conclusions HDAC1 in lung T cells may be involved in the pathogenesis of asthma.Histone modification by HDAC1 may be a specific eventwith gene transcription which may not be associated with asthma.

    Release date:2016-08-30 11:53 Export PDF Favorites Scan
  • Effects of Histone Modification on Chemokines Expression in Alveolar Epithelial TypeⅡ Cells in a RatModel of COPD

    Objective To investigate the effects of histone modification on the expression of chemokines in alveolar epithelial typeⅡ cells ( AECⅡ) in a rat model of chronic obstructive pulmonary disease ( COPD) . Methods 20 SD rats were randomly assigned to a normal control group and a COPD group. The rat model of COPD was established by cigarette smoking. Lung histological changes were observed by HE staining. AECⅡ cells were isolated and identified by alkaline phosphatase staining and electron microscopic. The mRNA expressions of monocyte chemoattractant protein ( MCP) -1, IL-8, and macrophage inflammatory protein ( MIP) -2αwere detected by real-time quantitative PCR. The expression of histone deacetylase ( HDAC) 2 was measured by western blot. Chromatin immunoprecipitation ( ChIP) was used todetect H3 and H4 acetylation, and H4K9 methylation in the promoter region of chemokine gene. Results Compared with the control group, the mRNA expressions of MCP-1, IL-8, and MIP-2αin the COPD group increased 4. 48,3. 14, and 2. 83 times, respectively. The expression of HDAC2 protein in the COPD group wassignificantly lower than in the control group ( 0. 25 ±0. 15 vs. 0. 66 ±0. 15, P lt; 0. 05) . The expression of HDAC2 had a negative correlation with the gene expressions of IL-8, MCP-1, and MIP-2α( r = - 0. 960,- 0. 914, - 0. 928, respectively, all P lt;0. 05) . The levels of H3 and H4 acetylation were higher, and H4K9 methylation level was lower in the promoter region of chemokine gene in the COPD group compared with the control group ( all P lt; 0. 05) . Conclusions MCP-1, IL-8, and MIP-2α participate and promote the lung inflammatory response in COPD. HDAC2-mediated histone modification may play an important role in COPD inflammation.

    Release date:2016-08-30 11:53 Export PDF Favorites Scan
  • Histone deacetylases 6 inhibitor 23BB alleviated myoglobin-induced endoplasmic reticulum stress in tubular epithelial cells

    ObjectiveTo investigate the protective effects and mechanism of selective histone deacetylases 6 (HDAC6) inhibitor 23BB in myoglobin-induced proximal tubular cell lines (HK-2).MethodsHK-2 cells were divided into 5 groups, including control group, myoglobin (200 μmol/L) group, myoglobin (200 μmol/L)+23BB (1.25 nmol/L) group, myoglobin (200 μmol/L)+4-phenylbutyric acid (2 mmol/L) group, and myoglobin (200 μmol/L)+23BB (1.25 nmol/L)+tunicamycin (25 ng/mL) group. Cells were collected at 24 hours after treatment. The endoplasmic reticulum (ER) stress-related gene mRNA level and marker protein expression were evaluated by RT-PCR and Western blotting, including glucose regulated protein 78 (GRP78), C/EBP homology protein (CHOP), inositol-requiring enzyme 1 (IRE1), PKR-like ER kinase (PERK), and activating transcription factor 6.ResultsIn in vitro study, ER stress-related mRNA of GRP78, IRE1α, PERK, and CHOP and marker protein expression of GRP78 and CHOP were found to increase in response to myoglobin treatment. Either administration of 23BB or 4-PBA could alleviate myoglobin-induced these changes.ConclusionThe protective effect of HDAC6 inhibitor 23BB is through the inhibition of myoglobin-induced ER stress in HK-2 cells.

    Release date:2018-07-27 09:54 Export PDF Favorites Scan
  • Relationship Between Histone Modifications and Gastrointestinal Cancer

    Objective To review the relationship between histone modifications and gastrointestinal cancer. Methods Literatures on histone modifications and the relationship between histone modifications and gastrointestinal cancer were collected and reviewed. Results Histone modifications played an important role in the establishment of gene silencing during tumorgenesis. DNA methylation and histone modifications might interact with each other and form a complex network to establish and maintain gene silencing. Restoring gene function silenced by epigenetic changes in cancer had the potential of ‘normalizing’ cancer cells, which was named epigenetic therapy. Epigenetic therapy was very promising in prevention and treatment of gastrointestinal cancer, but many unsolved issues remain which need to be addressed in future studies. Conclusion Histone modifications are associated with the pathogenesis of gastrointestinal cancer. Restoring gene function silenced by epigenetic changes may have a great role in the prevention and treatment of gastrointestinal cancer.

    Release date:2016-09-08 11:49 Export PDF Favorites Scan
  • 组蛋白H3F3A和H3F3B基因变异相关发育性癫痫性脑病二例并文献复习

    Release date:2025-07-22 10:02 Export PDF Favorites Scan
  • 癫痫与表观遗传学

    癫痫是一种以反复刻板性发作为特征的慢性神经系统疾病,现仍有20%~30%为难治性癫痫患儿,且发病机制尚未完全阐明。目前研究发现癫痫发病过程中存在表观遗传修饰异常,主要包括DNA甲基化、染色质重组、组蛋白修饰和非编码RNA调控等。文章将讨论表观遗传学在癫痫发病机制中的调控作用,以及与局灶性癫痫和全面性癫痫的关系,期待能从表观遗传学的角度阐明癫痫的发病机制,从而为癫痫药理学治疗分子靶标的识别提供新方向。

    Release date:2017-04-01 08:51 Export PDF Favorites Scan
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