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组蛋白高乙酰化介导的Egr-1结合促进gdnf基因高转录

李周儒 刘捷 雷宇 倪海波 蔡红星 张宝乐

南方医科大学学报Issue(5):697-701,5.
南方医科大学学报Issue(5):697-701,5.DOI:10.3969/j.issn.1673-4254.2015.05.14

组蛋白高乙酰化介导的Egr-1结合促进gdnf基因高转录

Increased Egr-1 binding to promoter induced by histone hyperacetylation promotes gdnf gene transcription

李周儒 1刘捷 2雷宇 2倪海波 3蔡红星 1张宝乐2

作者信息

  • 1. 徐州医学院 法医学教研室,江苏 徐州 221004
  • 2. 徐州医学院 生物学教研室,江苏 徐州 221004
  • 3. 苏州大学附属第一医院神经外科,江苏 苏州215006
  • 折叠

摘要

Abstract

Objective To investigate the mechanism of high transcription of the glial cell-line derived neurotrophic factor (gdnf) gene induced by hyperacetylation of histone H3 lysine 9 (H3K9) at its promoter region II in rat C6 glioma cells. Methods The acetylation level of H3K9 at Egr-1 binding site in gdnf gene promoter region II and the binding capacity of Egr-1 to its binding site in gdnf promoter were examined by ChIP-PCR in C6 astroglioma cells and normal rat astrocytes, and its changes were investigated in C6 astroglioma cells after treatment with histone acetyltransferase inhibitor curcumin or deacetylase inhibitor trichostatin A. Results Compared normal astrocytes, C6 astroglioma cells showed significantly increased acetylation level of H3K9 at Egr-1 binding site in gdnf gene promoter region II and Egr-1 binding capacity (P<0.01). Curcumin treatment significantly reduced H3K9 acetylation level at Egr-1 binding site and decreased both the binding of Egr-1 to promoter region II and gdnf mRNA levels in C6 astroglioma cells (P<0.05). Conversely, increased H3K9 acetylation at the Egr-1 binding site induced by trichostatin A significantly increased the binding of Egr-1 to promoter region II and gdnf mRNA expression levels (P<0.05). Conclusion H3K9 hyperacetylation induces increased Egr-1 binding to gdnf gene promoter II, which might be the reason for the high transcription level of gdnf gene in rat C6 glioma cells.

关键词

gdnf/启动子/组蛋白乙酰化/Egr-1/胶质瘤

Key words

gdnf/promoter/histone acetylation/Egr-1/glioma

引用本文复制引用

李周儒,刘捷,雷宇,倪海波,蔡红星,张宝乐..组蛋白高乙酰化介导的Egr-1结合促进gdnf基因高转录[J].南方医科大学学报,2015,(5):697-701,5.

基金项目

国家自然科学基金(31271358);江苏省自然科学青年基金(BK20130212);中国博士后基金(2013M540466) Supported by National Natural Science Foundation of China (31271358) (31271358)

南方医科大学学报

OA北大核心CSCDCSTPCDMEDLINE

1673-4254

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