张华莉

教授 博士生导师 硕士生导师

入职时间:1997-07-09

所在单位:基础医学院

学历:博士研究生毕业

办公地点:湘雅老校区第二教学楼5楼

性别:女

联系方式:15607310187

学位:医学博士学位

在职信息:在职

主要任职:湖南省脓毒症转化医学重点实验室学术委员会副主任,湖南省病理生理学会副理事长,危重病专业委员会副主任委员,中国病理生理学会常务理事

毕业院校:中南大学

学科:基础医学

曾获荣誉:

2013-06-01  当选:  中南大学“升华学者”特聘教授

2013-06-01  当选:  湖南省自然科学杰出青年基金获得者

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HSF1 Attenuates LPS-Induced Acute Lung Injury in Mice by Suppressing Macrophage Infiltration.

发布时间:2021-06-02

点击次数:

影响因子:5.076

发表刊物:Oxid Med Cell Longev .

摘要:Heat shock factor 1 (HSF1) is a transcription factor involved in the heat shock response and other biological processes. We have unveiled here an important role of HSF1 in acute lung injury (ALI). HSF1 knockout mice were used as a model of lipopolysaccharide- (LPS-) induced ALI. Lung damage was aggravated, and macrophage infiltration increased significantly in the bronchoalveolar lavage fluid (BALF) and lung tissue of HSF−/− mice compared with the damage observed in HSF1+/+ mice. Upon LPS stimulation, HSF−/− mice showed higher levels of monocyte chemoattractant protein-1 (MCP-1) in the serum, BALF, and lung tissue and increased the expression of MCP-1 and chemokine (C-C motif) receptor 2 (CCR2) on the surface of macrophages compared with those in HSF1+/+. Electrophoretic mobility shift assays (EMSA) and dual luciferase reporter assays revealed that HSF1 could directly bind to heat shock elements (HSE) in the promoter regions of MCP-1 and its receptor CCR2, thereby inhibiting the expression of both genes. We concluded that HSF1 attenuated LPS-induced ALI in mice by directly suppressing the transcription of MCP-1/CCR2, which in turn reduced macrophage infiltration.

合写作者:Sipin Tan,Xueyan Shi,Leijing Yin,Chuyi Tan,Jia Gu,Yanjuan Liu,Huafei Deng,Ke Liu,Meidong Liu

第一作者:Tao Li,Gui Xiao

论文类型:基础研究

通讯作者:Huali Zhang(通讯作者),?Xianzhong Xiao

学科门类:医学

一级学科:基础医学

期号:2020, 2020(9572):1-15.

是否译文:

发表时间:2020-12-18

收录刊物:SCI

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