PMID- 30336422
OWN - NLM
STAT- MEDLINE
DCOM- 20190114
LR  - 20200106
IS  - 2299-5684 (Electronic)
IS  - 1734-1140 (Linking)
VI  - 70
IP  - 6
DP  - 2018 Dec
TI  - Oleoylethanolamide alleviates macrophage formation via AMPK/PPARalpha/STAT3 pathway.
PG  - 1185-1194
LID - S1734-1140(17)30533-9 [pii]
LID - 10.1016/j.pharep.2018.06.006 [doi]
AB  - BACKGROUND: Atherosclerosis is the main underlying cause of most cardiovascular 
      diseases, and monocyte migrating to the vascular wall and subsequently 
      differentiating into macrophage are critical steps in the process of 
      atherosclerosis. The goal of this study was to clarify the effect of 
      oleoylethanolamide (OEA) on monocyte migration and subsequent macrophage 
      formation in the vascular wall. METHODS: We studied OEA in two monocyte-migrating 
      systems in vitro: one was a single cell system whereby monocytes were exposed to 
      OEA directly; the other was a co-culture system whereby monocytes were exposed to 
      OEA-treated macrophages. The effect of OEA on macrophage content in the vascular 
      wall in vivo was measured in apolipoprotein E (apoE)-/- mice by CD68 
      immunohistochemistry. The protein and mRNA expressions with OEA treatment were 
      examined using western blot and real-time PCR. RESULTS: Interestingly, OEA 
      possessed dual-directional regulation of monocyte chemotaxis in vitro, with a 
      stimulatory effect in the single cell system and a suppressive effect in the 
      co-culture system. And OEA restrained macrophage deposition in the vascular wall 
      of apoE-/- mice. The underlying mechanism of OEA suppressing monocyte migration 
      in the co-culture system was that OEA increased phosphorylation of AMP-activated 
      protein kinase (AMPK) and peroxisome proliferator-activated receptor alpha (PPARalpha) 
      level, and decreased phosphorylation of signal transducer and activator of 
      transcription 3 (STAT3) and monocyte chemoattractant protein-1 (MCP-1) level in 
      macrophages, which was reinforced by the in vivo experiment. CONCLUSIONS: OEA 
      restrains excessive macrophage formation in the progressive lesion by inhibiting 
      MCP-1 production of the existent macrophages through the AMPK/PPARalpha/STAT3 
      pathway.
CI  - Copyright (c) 2018 Institute of Pharmacology, Polish Academy of Sciences. Published 
      by Elsevier B.V. All rights reserved.
FAU - Zhao, Yun
AU  - Zhao Y
AD  - Xiamen Key Laboratory of Chiral Drugs, Medical College, Xiamen University, 
      Xiamen, China.
FAU - Yan, Lu
AU  - Yan L
AD  - Xiamen Key Laboratory of Chiral Drugs, Medical College, Xiamen University, 
      Xiamen, China.
FAU - Peng, Lu
AU  - Peng L
AD  - Xiamen Key Laboratory of Chiral Drugs, Medical College, Xiamen University, 
      Xiamen, China.
FAU - Huang, XueFeng
AU  - Huang X
AD  - Xiamen University Affiliated Zhongshan Hospital, Xiamen, China.
FAU - Zhang, GuiXiang
AU  - Zhang G
AD  - Xiamen Key Laboratory of Chiral Drugs, Medical College, Xiamen University, 
      Xiamen, China.
FAU - Chen, BingQian
AU  - Chen B
AD  - Xiamen Key Laboratory of Chiral Drugs, Medical College, Xiamen University, 
      Xiamen, China.
FAU - Ren, Jie
AU  - Ren J
AD  - Xiamen Key Laboratory of Chiral Drugs, Medical College, Xiamen University, 
      Xiamen, China.
FAU - Zhou, Yu
AU  - Zhou Y
AD  - Xiamen Key Laboratory of Chiral Drugs, Medical College, Xiamen University, 
      Xiamen, China.
FAU - Yang, LiChao
AU  - Yang L
AD  - Xiamen Key Laboratory of Chiral Drugs, Medical College, Xiamen University, 
      Xiamen, China.
FAU - Peng, Li
AU  - Peng L
AD  - Xiamen Key Laboratory of Chiral Drugs, Medical College, Xiamen University, 
      Xiamen, China.
FAU - Jin, Xin
AU  - Jin X
AD  - Xiamen Key Laboratory of Chiral Drugs, Medical College, Xiamen University, 
      Xiamen, China. Electronic address: xinjin@xmu.edu.cn.
FAU - Wang, YiQing
AU  - Wang Y
AD  - Xiamen University Affiliated Zhongshan Hospital, Xiamen, China. Electronic 
      address: wang_gina@163.com.
LA  - eng
PT  - Journal Article
DEP - 20180623
PL  - Switzerland
TA  - Pharmacol Rep
JT  - Pharmacological reports : PR
JID - 101234999
RN  - 0 (Endocannabinoids)
RN  - 0 (Oleic Acids)
RN  - 0 (PPAR alpha)
RN  - 0 (STAT3 Transcription Factor)
RN  - 0 (Stat3 protein, mouse)
RN  - 1HI5J9N8E6 (oleoylethanolamide)
RN  - EC 2.7.11.31 (AMP-Activated Protein Kinases)
SB  - IM
MH  - AMP-Activated Protein Kinases/*metabolism
MH  - Animals
MH  - Cells, Cultured
MH  - Dose-Response Relationship, Drug
MH  - Endocannabinoids/*pharmacology
MH  - Humans
MH  - Macrophages/drug effects/*metabolism
MH  - Male
MH  - Mice
MH  - Mice, 129 Strain
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Oleic Acids/*pharmacology
MH  - PPAR alpha/*metabolism
MH  - Random Allocation
MH  - STAT3 Transcription Factor/antagonists & inhibitors/*metabolism
MH  - Signal Transduction/*drug effects/physiology
MH  - THP-1 Cells
OTO - NOTNLM
OT  - AMPK
OT  - Macrophage formation
OT  - Monocyte migration
OT  - Oleoylethanolamide
OT  - PPARalpha
EDAT- 2018/10/20 06:00
MHDA- 2019/01/15 06:00
CRDT- 2018/10/19 06:00
PHST- 2017/07/29 00:00 [received]
PHST- 2018/06/08 00:00 [revised]
PHST- 2018/06/22 00:00 [accepted]
PHST- 2018/10/20 06:00 [pubmed]
PHST- 2019/01/15 06:00 [medline]
PHST- 2018/10/19 06:00 [entrez]
AID - S1734-1140(17)30533-9 [pii]
AID - 10.1016/j.pharep.2018.06.006 [doi]
PST - ppublish
SO  - Pharmacol Rep. 2018 Dec;70(6):1185-1194. doi: 10.1016/j.pharep.2018.06.006. Epub 
      2018 Jun 23.