PMID- 33831591
OWN - NLM
STAT- MEDLINE
DCOM- 20210927
LR  - 20210927
IS  - 1878-5875 (Electronic)
IS  - 1357-2725 (Linking)
VI  - 135
DP  - 2021 Jun
TI  - SNF5 promotes IL-1beta expression via H3K4me1 in atherosclerosis induced by 
      homocysteine.
PG  - 105974
LID - S1357-2725(21)00058-3 [pii]
LID - 10.1016/j.biocel.2021.105974 [doi]
AB  - Homocysteine (Hcy) is a strong and independent risk factor of atherosclerosis. It 
      can accelerate atherosclerosis through increased production of inflammatory 
      factors, especially interleukin-1 beta (IL-1beta), while the precise mechanisms remain 
      to be well elucidated. In this study, we investigated the role of the tumor 
      suppressor gene SNF5 related to switch/sucrose non-fermentable complex (SWI/SNF) 
      in the occurrence and development of atherosclerosis induced by Hcy. Using 
      Hyperhomocysteinemia (HHcy) atherosclerotic model with apolipoprotein E knockout 
      (ApoE(-/-)) mice fed with high-methionine diet, we showed that Hcy aggravates 
      inflammation in macrophages during the atherosclerotic plaque formation. Further 
      analysis showed that SNF5 promotes IL-1beta expression and secretion. In addition, 
      due to the existence of H3K4 methylation signals in the vicinity of IL-1beta, we 
      found that Hcy significantly promotes the expression of H3K4me1, and 
      lysine-specific histone demethylase 1A (KDM1A) acts as a transcriptional 
      repressor to regulate the expression of H3K4me1 by demethylating H3K4me1. In 
      summary, our results demonstrated that Hcy up-regulates the expression of SNF5 
      through KDM1A, resulting in an increased level of H3K4me1 modification and IL-1beta 
      in macrophages, which in turn promotes the formation of atherosclerosis. Our 
      study will provide more evidence for further revealing the specific mechanism of 
      Hcy-induced inflammation and the diagnosis, prevention, and treatment of 
      atherosclerosis.
CI  - Copyright (c) 2021 The Authors. Published by Elsevier Ltd.. All rights reserved.
FAU - Xie, Lin
AU  - Xie L
AD  - School of Basic Medical Sciences, Ningxia Medical University, Yinchuan, 750004, 
      China; NHC Key Laboratory of Metabolic Cardiovascular Diseases Research, Ningxia 
      Medical University, Yinchuan, 750004, China; Ningxia Key Laboratory of Vascular 
      Injury and Repair Research, Ningxia Medical University, Yinchuan, 750004, China.
FAU - Ding, Ning
AU  - Ding N
AD  - School of Basic Medical Sciences, Ningxia Medical University, Yinchuan, 750004, 
      China; NHC Key Laboratory of Metabolic Cardiovascular Diseases Research, Ningxia 
      Medical University, Yinchuan, 750004, China; Ningxia Key Laboratory of Vascular 
      Injury and Repair Research, Ningxia Medical University, Yinchuan, 750004, China.
FAU - Zhang, Honghong
AU  - Zhang H
AD  - School of Basic Medical Sciences, Ningxia Medical University, Yinchuan, 750004, 
      China; NHC Key Laboratory of Metabolic Cardiovascular Diseases Research, Ningxia 
      Medical University, Yinchuan, 750004, China; Ningxia Key Laboratory of Vascular 
      Injury and Repair Research, Ningxia Medical University, Yinchuan, 750004, China.
FAU - Liu, Kun
AU  - Liu K
AD  - NHC Key Laboratory of Metabolic Cardiovascular Diseases Research, Ningxia Medical 
      University, Yinchuan, 750004, China; Ningxia Key Laboratory of Vascular Injury 
      and Repair Research, Ningxia Medical University, Yinchuan, 750004, China; 
      Department of Clinical Medicine, Ningxia Medical University, Yinchuan, 750004, 
      China.
FAU - Xiong, Jiantuan
AU  - Xiong J
AD  - School of Basic Medical Sciences, Ningxia Medical University, Yinchuan, 750004, 
      China; NHC Key Laboratory of Metabolic Cardiovascular Diseases Research, Ningxia 
      Medical University, Yinchuan, 750004, China; Ningxia Key Laboratory of Vascular 
      Injury and Repair Research, Ningxia Medical University, Yinchuan, 750004, China.
FAU - Ma, Shengchao
AU  - Ma S
AD  - School of Basic Medical Sciences, Ningxia Medical University, Yinchuan, 750004, 
      China; NHC Key Laboratory of Metabolic Cardiovascular Diseases Research, Ningxia 
      Medical University, Yinchuan, 750004, China; Ningxia Key Laboratory of Vascular 
      Injury and Repair Research, Ningxia Medical University, Yinchuan, 750004, China.
FAU - Yang, Anning
AU  - Yang A
AD  - School of Basic Medical Sciences, Ningxia Medical University, Yinchuan, 750004, 
      China; NHC Key Laboratory of Metabolic Cardiovascular Diseases Research, Ningxia 
      Medical University, Yinchuan, 750004, China; Ningxia Key Laboratory of Vascular 
      Injury and Repair Research, Ningxia Medical University, Yinchuan, 750004, China.
FAU - Zhang, Huiping
AU  - Zhang H
AD  - NHC Key Laboratory of Metabolic Cardiovascular Diseases Research, Ningxia Medical 
      University, Yinchuan, 750004, China; Ningxia Key Laboratory of Vascular Injury 
      and Repair Research, Ningxia Medical University, Yinchuan, 750004, China; 
      Prenatal Diagnosis Center of General Hospital, Ningxia Medical University, 
      Yinchuan, 750004, China. Electronic address: zhp19760820@163.com.
FAU - Jiang, Yideng
AU  - Jiang Y
AD  - School of Basic Medical Sciences, Ningxia Medical University, Yinchuan, 750004, 
      China; NHC Key Laboratory of Metabolic Cardiovascular Diseases Research, Ningxia 
      Medical University, Yinchuan, 750004, China; Ningxia Key Laboratory of Vascular 
      Injury and Repair Research, Ningxia Medical University, Yinchuan, 750004, China. 
      Electronic address: jydeng@nxmu.edu.cn.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20210405
PL  - Netherlands
TA  - Int J Biochem Cell Biol
JT  - The international journal of biochemistry & cell biology
JID - 9508482
RN  - 0 (Histones)
RN  - 0 (IL1B protein, mouse)
RN  - 0 (Interleukin-1beta)
RN  - 0 (SMARCB1 Protein)
RN  - 0 (Smarcb1 protein, mouse)
RN  - 0LVT1QZ0BA (Homocysteine)
SB  - IM
MH  - Animals
MH  - Atherosclerosis/chemically induced/metabolism/*pathology
MH  - Gene Expression Regulation/*drug effects
MH  - Histones/genetics/*metabolism
MH  - Homocysteine/*toxicity
MH  - Inflammation/*complications
MH  - Interleukin-1beta/genetics/*metabolism
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout, ApoE
MH  - SMARCB1 Protein/genetics/*metabolism
OTO - NOTNLM
OT  - Atherosclerosis
OT  - H3K4me1
OT  - Homocysteine
OT  - IL-1beta
OT  - SNF5
EDAT- 2021/04/09 06:00
MHDA- 2021/09/28 06:00
CRDT- 2021/04/08 20:19
PHST- 2020/11/28 00:00 [received]
PHST- 2021/03/29 00:00 [revised]
PHST- 2021/03/31 00:00 [accepted]
PHST- 2021/04/09 06:00 [pubmed]
PHST- 2021/09/28 06:00 [medline]
PHST- 2021/04/08 20:19 [entrez]
AID - S1357-2725(21)00058-3 [pii]
AID - 10.1016/j.biocel.2021.105974 [doi]
PST - ppublish
SO  - Int J Biochem Cell Biol. 2021 Jun;135:105974. doi: 10.1016/j.biocel.2021.105974. 
      Epub 2021 Apr 5.