Journal:Inflammation .
Abstract:The heat shock transcription factor (HSF) is an important transactivator of the heat shock genes. Recent studies have shown that HSF1 acts as a repressor of non-heat shock genes to protect against endotoxemia. In this study, we found that heat shock treatment and HSF1 over-expression augmented the induction of interleukin (IL)-10 mRNA. Computational analysis of the mouse IL-10 promoter region showed that three potential heat shock elements (HSEs) were located at mouse IL-10 gene promoter, among which only the −387/−360 probe formed a complex with HSF1. The lack of binding of the other two HSEs to HSF1 suggested the critical role of the flanking sequences in the binding specificity of HSE to HSF1. Moreover, we showed that HSF1 overexpression transactivated mouse IL-10 gene promoter and this transcriptional activation was inhibited by the mutation of HSE in the −387/−360 region of IL-10 gene promoter using luciferase reporter assay. These findings indicate that HSF1 is a transcriptional activator of anti-inflammatory mediator IL-10 gene in RAW264.7 macrophages.
Co-author:Lingli Zhang,Fengxiu Yu,Ying Liu,Qiujuan Liang,Gonghua Deng,Guangwen Chen,Meidong Liu
First Author:Huali Zhang（第一作者）
Indexed by:Unit Twenty Basic Research
Correspondence Author:Xianzhong Xiao
Discipline:Medicine
First-Level Discipline:Basic Medicine
Issue:2012, 35(4):1558-66
Translation or Not:no
Included Journals:SCI