Epigenetic programming of diverse glucocorticoid response and inflammatory/immune-mediated disease

被引：21
作者：
Chen, Peisong [1 ]
Jiang, Tang [1 ]
Ouyang, Juan [1 ]
Cui, Yingpeng [1 ]
Chen, Yili [1 ]
机构：
[1] Sun Yat Sen Univ, Affiliated Hosp 1, Dept Lab Med, Guangzhou 510275, Guangdong, Peoples R China
来源：
MEDICAL HYPOTHESES | 2009年 / 73卷 / 05期
关键词：
RECEPTOR GENE; 1A PROMOTER; EXPRESSION; MECHANISMS; METHYLATION; RESISTANCE; IDENTIFICATION; SENSITIVITY; NR3C1; RATS;
D O I：
10.1016/j.mehy.2009.08.013
中图分类号：
R-3 [医学研究方法]; R3 [基础医学];
学科分类号：
1001 ;
摘要：
Glucocorticoid plays a fundamental role in maintaining immune homeostasis. Resistance to glucocorticoids is a potential etiology of inflammatory/immune-mediated disease. Most of the glucocorticoid effects are mediated by glucocorticoid receptor (GR), which has a complicated promoter region with multiple promoters. Studies have found that the methylation pattern of GR promoter is highly individual, which may contribute to the diverse glucocorticoid responds. Early life is a critical time for epigenetic programming of the body in which methylation imprints are established. Here we propose a hypothesis that connects the adverse early life events and the development of inflammatory/immune-mediated disease through an epigenetic mechanism, the methylation of GR gene. (C) 2009 Elsevier Ltd. All rights reserved.
引用
收藏
页码：657 / 658
页数：2
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