PMID- 33381262
OWN - NLM
STAT- MEDLINE
DCOM- 20210902
LR  - 20210902
IS  - 1942-0994 (Electronic)
IS  - 1942-0900 (Print)
IS  - 1942-0994 (Linking)
VI  - 2020
DP  - 2020
TI  - HSF1 Attenuates LPS-Induced Acute Lung Injury in Mice by Suppressing Macrophage 
      Infiltration.
PG  - 1936580
LID - 10.1155/2020/1936580 [doi]
LID - 1936580
AB  - 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.
CI  - Copyright (c) 2020 Tao Li et al.
FAU - Li, Tao
AU  - Li T
AD  - Key Laboratory of Sepsis Translational Medicine of Hunan, Department of 
      Pathophysiology, Xiangya School of Medicine, Central South University, Changsha, 
      Hunan 410008, China.
AD  - Department of Pathophysiology, Medical College of Jiaying University, Meizhou, 
      Guangdong 514031, China.
FAU - Xiao, Gui
AU  - Xiao G
AD  - Key Laboratory of Sepsis Translational Medicine of Hunan, Department of 
      Pathophysiology, Xiangya School of Medicine, Central South University, Changsha, 
      Hunan 410008, China.
AD  - Department of Nursing, Hainan Medical University, Haikou, Hainan 571199, China.
FAU - Tan, Sipin
AU  - Tan S
AD  - Key Laboratory of Sepsis Translational Medicine of Hunan, Department of 
      Pathophysiology, Xiangya School of Medicine, Central South University, Changsha, 
      Hunan 410008, China.
FAU - Shi, Xueyan
AU  - Shi X
AD  - Key Laboratory of Sepsis Translational Medicine of Hunan, Department of 
      Pathophysiology, Xiangya School of Medicine, Central South University, Changsha, 
      Hunan 410008, China.
FAU - Yin, Leijing
AU  - Yin L
AD  - Key Laboratory of Sepsis Translational Medicine of Hunan, Department of 
      Pathophysiology, Xiangya School of Medicine, Central South University, Changsha, 
      Hunan 410008, China.
FAU - Tan, Chuyi
AU  - Tan C
AD  - Key Laboratory of Sepsis Translational Medicine of Hunan, Department of 
      Pathophysiology, Xiangya School of Medicine, Central South University, Changsha, 
      Hunan 410008, China.
FAU - Gu, Jia
AU  - Gu J
AD  - Key Laboratory of Sepsis Translational Medicine of Hunan, Department of 
      Pathophysiology, Xiangya School of Medicine, Central South University, Changsha, 
      Hunan 410008, China.
FAU - Liu, Yanjuan
AU  - Liu Y
AD  - Key Laboratory of Sepsis Translational Medicine of Hunan, Department of 
      Pathophysiology, Xiangya School of Medicine, Central South University, Changsha, 
      Hunan 410008, China.
FAU - Deng, Huafei
AU  - Deng H
AD  - Key Laboratory of Sepsis Translational Medicine of Hunan, Department of 
      Pathophysiology, Xiangya School of Medicine, Central South University, Changsha, 
      Hunan 410008, China.
FAU - Liu, Ke
AU  - Liu K
AD  - Key Laboratory of Sepsis Translational Medicine of Hunan, Department of 
      Pathophysiology, Xiangya School of Medicine, Central South University, Changsha, 
      Hunan 410008, China.
FAU - Liu, Meidong
AU  - Liu M
AD  - Key Laboratory of Sepsis Translational Medicine of Hunan, Department of 
      Pathophysiology, Xiangya School of Medicine, Central South University, Changsha, 
      Hunan 410008, China.
FAU - Zhang, Huali
AU  - Zhang H
AUID- ORCID: 0000-0002-0788-7092
AD  - Key Laboratory of Sepsis Translational Medicine of Hunan, Department of 
      Pathophysiology, Xiangya School of Medicine, Central South University, Changsha, 
      Hunan 410008, China.
FAU - Xiao, Xianzhong
AU  - Xiao X
AUID- ORCID: 0000-0001-6706-8665
AD  - Key Laboratory of Sepsis Translational Medicine of Hunan, Department of 
      Pathophysiology, Xiangya School of Medicine, Central South University, Changsha, 
      Hunan 410008, China.
LA  - eng
PT  - Journal Article
DEP - 20201218
PL  - United States
TA  - Oxid Med Cell Longev
JT  - Oxidative medicine and cellular longevity
JID - 101479826
RN  - 0 (Heat Shock Transcription Factors)
RN  - 0 (Hsf1 protein, mouse)
RN  - 0 (Lipopolysaccharides)
SB  - IM
MH  - Acute Lung Injury/chemically induced/*genetics/immunology/pathology
MH  - Animals
MH  - Capillary Permeability/genetics
MH  - Cell Movement/genetics
MH  - Female
MH  - Heat Shock Transcription Factors/*physiology
MH  - Lipopolysaccharides
MH  - Lung/immunology/metabolism/pathology
MH  - Macrophages/pathology/*physiology
MH  - Male
MH  - Mice
MH  - Mice, Knockout
MH  - RAW 264.7 Cells
PMC - PMC7762676
COIS- The authors declare no conflict of interest, and the work described here has not 
      been published previously and not under consideration for publication elsewhere, 
      in whole or in part.
EDAT- 2021/01/01 06:00
MHDA- 2021/09/03 06:00
PMCR- 2020/12/18
CRDT- 2020/12/31 05:25
PHST- 2020/04/02 00:00 [received]
PHST- 2020/06/21 00:00 [revised]
PHST- 2020/12/01 00:00 [accepted]
PHST- 2020/12/31 05:25 [entrez]
PHST- 2021/01/01 06:00 [pubmed]
PHST- 2021/09/03 06:00 [medline]
PHST- 2020/12/18 00:00 [pmc-release]
AID - 10.1155/2020/1936580 [doi]
PST - epublish
SO  - Oxid Med Cell Longev. 2020 Dec 18;2020:1936580. doi: 10.1155/2020/1936580. 
      eCollection 2020.