PMID- 25299192
OWN - NLM
STAT- MEDLINE
DCOM- 20150622
LR  - 20141010
IS  - 1676-5680 (Electronic)
IS  - 1676-5680 (Linking)
VI  - 13
IP  - 4
DP  - 2014 Oct 7
TI  - Monocyte/macrophage beta2-AR as a target of antisympathetic excitation-induced 
      atherosclerotic progression.
PG  - 8080-8
LID - 10.4238/2014.October.7.2 [doi]
AB  - The aim of this study was to determine whether monocyte/macrophage beta2-AR could 
      act as the therapeutic target of antisympathetic excitation-induced 
      atherosclerotic progression. Cultivated human THP-1 cells were divided into 
      different groups and incubated with isoprenaline, metoprolol, propranolol or 
      beta2-AR blocker for 24 h, together with oxidized low-density lipoprotein (ox-LDL). 
      Afterwards, each group was analyzed for C-C chemokine receptor type 2 (CCR2) 
      expression, monocyte chemotactic protein 1 (MCP-1) release into medium and cell 
      migration ability. In the isoprenaline group, CCR2 protein level was increased, 
      as well as the secretion of MCP-1, and cell motility was enhanced, in a 
      concentration-dependent manner. Propranolol and ICI 118,551 significantly 
      reversed the stimulatory effect of isoprenaline on THP-1 cells induced by ox-LDL, 
      but only high concentrations of metoprolol interfered significantly with the 
      action of isoprenaline (P < 0.05). Isoprenaline or a beta-AR blocker could mediate 
      through beta2-AR, affecting MCP-1 secretion, CCR2 protein expression and cell 
      migration capacity of THP-1 cells. Therefore, monocyte-macrophage beta2-AR may act 
      as a target of antisympathetic excitation-induced atherosclerotic progression.
FAU - Guo, Y L
AU  - Guo YL
AD  - Cardiovascular Internal Department, Renhe Hospital, Three Gorges University, 
      Yichang, Hubei, China.
FAU - Zhou, J Q
AU  - Zhou JQ
AD  - Cardiovascular Internal Department, Renhe Hospital, Three Gorges University, 
      Yichang, Hubei, China jingqunzhou@163.com.
FAU - Xiang, C Q
AU  - Xiang CQ
AD  - Cardiovascular Internal Department, Renhe Hospital, Three Gorges University, 
      Yichang, Hubei, China.
FAU - Yang, W H
AU  - Yang WH
AD  - Cardiovascular Internal Department, Renhe Hospital, Three Gorges University, 
      Yichang, Hubei, China.
FAU - Zhang, B
AU  - Zhang B
AD  - Cardiovascular Internal Department, Renhe Hospital, Three Gorges University, 
      Yichang, Hubei, China.
FAU - Dai, W J
AU  - Dai WJ
AD  - Cardiovascular Internal Department, Renhe Hospital, Three Gorges University, 
      Yichang, Hubei, China.
FAU - Liu, J H
AU  - Liu JH
AD  - Cardiovascular Internal Department, Renhe Hospital, Three Gorges University, 
      Yichang, Hubei, China.
FAU - Zheng, S J
AU  - Zheng SJ
AD  - Cardiovascular Internal Department, Renhe Hospital, Three Gorges University, 
      Yichang, Hubei, China.
LA  - eng
PT  - Journal Article
DEP - 20141007
PL  - Brazil
TA  - Genet Mol Res
JT  - Genetics and molecular research : GMR
JID - 101169387
RN  - 0 (Adrenergic beta-1 Receptor Antagonists)
RN  - 0 (Adrenergic beta-2 Receptor Antagonists)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Receptors, Adrenergic, beta-2)
RN  - 0 (Receptors, CCR2)
RN  - 0 (Sympatholytics)
SB  - IM
MH  - Adrenergic beta-1 Receptor Antagonists/pharmacology
MH  - Adrenergic beta-2 Receptor Antagonists/*pharmacology
MH  - Atherosclerosis/*etiology/*metabolism/pathology
MH  - Cell Line
MH  - Cell Movement/drug effects
MH  - Cells, Cultured
MH  - Chemokine CCL2/metabolism
MH  - Disease Progression
MH  - Humans
MH  - Macrophages/*metabolism
MH  - Monocytes/*metabolism
MH  - Receptors, Adrenergic, beta-2/*metabolism
MH  - Receptors, CCR2/metabolism
MH  - Sympatholytics/*pharmacology
EDAT- 2014/10/10 06:00
MHDA- 2015/06/24 06:00
CRDT- 2014/10/10 06:00
PHST- 2014/10/10 06:00 [entrez]
PHST- 2014/10/10 06:00 [pubmed]
PHST- 2015/06/24 06:00 [medline]
AID - gmr3762 [pii]
AID - 10.4238/2014.October.7.2 [doi]
PST - epublish
SO  - Genet Mol Res. 2014 Oct 7;13(4):8080-8. doi: 10.4238/2014.October.7.2.