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Genet Mol Res. 2014 Oct 7;13(4):8080-8. doi: 10.4238/2014.October.7.2.

Monocyte/macrophage β2-AR as a target of antisympathetic excitation-induced atherosclerotic progression.

Author information

1
Cardiovascular Internal Department, Renhe Hospital, Three Gorges University, Yichang, Hubei, China.
2
Cardiovascular Internal Department, Renhe Hospital, Three Gorges University, Yichang, Hubei, China jingqunzhou@163.com.

Abstract

The aim of this study was to determine whether monocyte/macrophage β2-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 β2-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 β-AR blocker could mediate through β2-AR, affecting MCP-1 secretion, CCR2 protein expression and cell migration capacity of THP-1 cells. Therefore, monocyte-macrophage β2-AR may act as a target of antisympathetic excitation-induced atherosclerotic progression.

PMID:
25299192
DOI:
10.4238/2014.October.7.2
[Indexed for MEDLINE]
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