PMID- 29570119
OWN - NLM
STAT- MEDLINE
DCOM- 20200423
LR  - 20210103
IS  - 1540-0514 (Electronic)
IS  - 1073-2322 (Linking)
VI  - 51
IP  - 3
DP  - 2019 Mar
TI  - H3K4 Methylation Regulates LPS-Induced Proinflammatory Cytokine Expression and 
      Release in Macrophages.
PG  - 401-406
LID - 10.1097/SHK.0000000000001141 [doi]
AB  - Histone methylation is an important epigenetic mechanism that plays an essential 
      role in regulating gene expression in mammalian cells. To understand its 
      influence on inflammation, methylation of H3K4, H3K9, H3K36, H3K79, and H4K20, 
      the most common histones methylated in the inflammatory response was analyzed in 
      murine RAW264.7 cells and bone marrow-derived macrophages (BMDMs) upon 
      lipopolysaccharide (LPS) stimulation. LPS stimulation resulted in enhanced 
      methylation at H3K4 and H3K9 in both RAW264.7 and BMDMs. To further confirm 
      whether LPS-stimulated H3K4me2 and H3K9me2 were responsible for subsequent 
      proinflammatory cytokine expression, the recruitment of H3K4me2 and H3K9me2 at 
      the promoters of interleukin (IL)-6 and tumor necrosis factor-alpha (TNF-alpha) was 
      assessed. H3K4me2, but not H3K9me2, was enriched at the promoters of both IL-6 
      and TNF-alpha. Furthermore, LPS-stimulated gene expression and release of IL-6 and 
      TNF-alpha were markedly suppressed in macrophages by MTA, a specific inhibitor of 
      H3K4 methylation. These results demonstrate that histone methylation, in 
      particular H3K4me2, plays a critical role in the regulation of LPS-induced 
      expression and release of IL-6 and TNF-alpha.
FAU - Zhao, Shuqi
AU  - Zhao S
AD  - Guangdong Provincial Key Laboratory of Proteomics, School of Basic Medical 
      Sciences, Southern Medical University, Guangzhou, China.
FAU - Zhong, Yuyun
AU  - Zhong Y
FAU - Fu, Xiaoxia
AU  - Fu X
FAU - Wang, Yiqian
AU  - Wang Y
FAU - Ye, Ping
AU  - Ye P
FAU - Cai, Junwei
AU  - Cai J
FAU - Liu, Yun
AU  - Liu Y
FAU - Sun, Jiang
AU  - Sun J
FAU - Mei, Zhuzhong
AU  - Mei Z
FAU - Jiang, Yong
AU  - Jiang Y
FAU - Liu, Jinghua
AU  - Liu J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Shock
JT  - Shock (Augusta, Ga.)
JID - 9421564
RN  - 0 (Histones)
RN  - 0 (Interleukin-6)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (interleukin-6, mouse)
RN  - 0 (lipopolysaccharide, Escherichia coli O111 B4)
SB  - IM
MH  - Animals
MH  - Gene Expression Regulation/*drug effects
MH  - Histones/*metabolism
MH  - Inflammation/chemically induced/metabolism/pathology
MH  - Interleukin-6/*biosynthesis
MH  - Lipopolysaccharides/*toxicity
MH  - Macrophages/*metabolism/pathology
MH  - Male
MH  - Methylation/drug effects
MH  - Mice
MH  - Protein Processing, Post-Translational/*drug effects
MH  - RAW 264.7 Cells
MH  - Tumor Necrosis Factor-alpha/*biosynthesis
EDAT- 2018/03/24 06:00
MHDA- 2020/04/24 06:00
CRDT- 2018/03/24 06:00
PHST- 2018/03/24 06:00 [pubmed]
PHST- 2020/04/24 06:00 [medline]
PHST- 2018/03/24 06:00 [entrez]
AID - 10.1097/SHK.0000000000001141 [doi]
PST - ppublish
SO  - Shock. 2019 Mar;51(3):401-406. doi: 10.1097/SHK.0000000000001141.