title: Monocyte/macrophage β2-AR as a target of antisympathetic excitation-induced atherosclerotic progression.
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.
authors.affiliation: Cardiovascular Internal Department, Renhe Hospital, Three Gorges University, Yichang, Hubei, China.
authors.forename: Y L
authors.initials: YL
authors.lastname: Guo
authors.affiliation: Cardiovascular Internal Department, Renhe Hospital, Three Gorges University, Yichang, Hubei, China jingqunzhou@163.com.
authors.forename: J Q
authors.initials: JQ
authors.lastname: Zhou
authors.affiliation: Cardiovascular Internal Department, Renhe Hospital, Three Gorges University, Yichang, Hubei, China.
authors.forename: C Q
authors.initials: CQ
authors.lastname: Xiang
authors.affiliation: Cardiovascular Internal Department, Renhe Hospital, Three Gorges University, Yichang, Hubei, China.
authors.forename: W H
authors.initials: WH
authors.lastname: Yang
authors.affiliation: Cardiovascular Internal Department, Renhe Hospital, Three Gorges University, Yichang, Hubei, China.
authors.forename: B
authors.initials: B
authors.lastname: Zhang
authors.affiliation: Cardiovascular Internal Department, Renhe Hospital, Three Gorges University, Yichang, Hubei, China.
authors.forename: W J
authors.initials: WJ
authors.lastname: Dai
authors.affiliation: Cardiovascular Internal Department, Renhe Hospital, Three Gorges University, Yichang, Hubei, China.
authors.forename: J H
authors.initials: JH
authors.lastname: Liu
authors.affiliation: Cardiovascular Internal Department, Renhe Hospital, Three Gorges University, Yichang, Hubei, China.
authors.forename: S J
authors.initials: SJ
authors.lastname: Zheng
mesh_terms: D058671:Adrenergic beta-1 Receptor Antagonists / Q000494:pharmacology; D058672:Adrenergic beta-2 Receptor Antagonists / Q000494:pharmacology*; D050197:Atherosclerosis / Q000209:etiology* / Q000378:metabolism* / Q000473:pathology; D002460:Cell Line; D002465:Cell Movement / Q000187:drug effects; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000378:metabolism; D018450:Disease Progression; D006801:Humans; D008264:Macrophages / Q000378:metabolism*; D009000:Monocytes / Q000378:metabolism*; D018343:Receptors, Adrenergic, beta-2 / Q000378:metabolism*; D054390:Receptors, CCR2 / Q000378:metabolism; D013565:Sympatholytics / Q000494:pharmacology*
chemical_list: D058671:Adrenergic beta-1 Receptor Antagonists; D058672:Adrenergic beta-2 Receptor Antagonists; D018932:Chemokine CCL2; D018343:Receptors, Adrenergic, beta-2; D054390:Receptors, CCR2; D013565:Sympatholytics