PMID- 29609686
OWN - NLM
STAT- MEDLINE
DCOM- 20181218
LR  - 20181218
IS  - 0031-7144 (Print)
IS  - 0031-7144 (Linking)
VI  - 73
IP  - 4
DP  - 2018 Apr 2
TI  - Aberrant histone modifications of global histone and MCP-1 promoter in CD14(+) 
      monocytes from patients with coronary artery disease.
PG  - 202-206
LID - 10.1691/ph.2018.7342 [doi]
AB  - OBJECTIVES: To investigate whether there are aberrant acetylation modifications 
      in global histone and monocyte chemoattractant protein-1 (MCP-1) promoter in 
      monocytes from patients with coronary artery disease (CAD) and demonstrate the 
      potential mechanisms. METHODS: CD14+ monocytes were isolated from 13 patients 
      with CAD and 18 confirmed non-CAD controls using magnetic beads. Global histone 
      H3/H4 acetylation and H3K4/H3K27 tri-methylation levels were measured with 
      enzyme-linked immunosorbent assay. Quantitative real time-PCR was performed to 
      detect the mRNA expression levels of MCP-1 and enzymes involved in histone 
      modification processes. Histone modification levels in MCP-1 promoter were 
      assessed by ChIP-qPCR assay. RESULTS: Our results showed a markedly lower global 
      histone H3 acetylation level in monocytes from CAD patients. Global H3K27 
      tri-methylation level was significantly increased in monocytes from CAD patients. 
      Furthermore, the mRNA expression levels of epigenetic modification enzymes HDAC3, 
      SIRT1, P300, JMJD3 and SUV39H1 were decreased significantly in monocytes from CAD 
      patients, while HDAC7 mRNA expression level was markedly increased. MCP-1 mRNA 
      expression level was increased histone H3/H4 acetylation levels in MCP-1 promoter 
      were markedly increased in monocytes of CAD patients. CONCLUSION: Aberrant 
      histone modifications, including acetylation and tri-methylation, were found both 
      in global histone and specific MCP-1 gene locos in monocytes from patients with 
      CAD. Aberrant epigenetic modification enzymes expressions may be the regulatory 
      mechanism responsible for aberrant histone modifications.
FAU - Xiao, L I
AU  - Xiao LI
FAU - Cao, Yu
AU  - Cao Y
FAU - Wang, Yang
AU  - Wang Y
FAU - Lai, Xin
AU  - Lai X
FAU - Gao, Ke-Qin
AU  - Gao KQ
FAU - Du, Pei
AU  - Du P
FAU - Zhang, Bi-Kui
AU  - Zhang BK
FAU - Jia, Su-Jie
AU  - Jia SJ
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Germany
TA  - Pharmazie
JT  - Die Pharmazie
JID - 9800766
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Histones)
RN  - 0 (Lipopolysaccharide Receptors)
SB  - IM
MH  - Acetylation
MH  - Chemokine CCL2/*genetics
MH  - Coronary Artery Disease/*genetics/*metabolism
MH  - Female
MH  - Histones/chemistry/genetics/*metabolism
MH  - Humans
MH  - Lipopolysaccharide Receptors/*genetics/*metabolism
MH  - Male
MH  - Middle Aged
MH  - Monocytes/enzymology/*metabolism
MH  - Promoter Regions, Genetic
MH  - Protein Processing, Post-Translational
EDAT- 2018/04/04 06:00
MHDA- 2018/12/19 06:00
CRDT- 2018/04/04 06:00
PHST- 2018/04/04 06:00 [entrez]
PHST- 2018/04/04 06:00 [pubmed]
PHST- 2018/12/19 06:00 [medline]
AID - 10.1691/ph.2018.7342 [doi]
PST - ppublish
SO  - Pharmazie. 2018 Apr 2;73(4):202-206. doi: 10.1691/ph.2018.7342.