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

被引:10
作者
Guo, Y. L. [1 ]
Zhou, J. Q. [1 ]
Xiang, C. Q. [1 ]
Yang, W. H. [1 ]
Zhang, B. [1 ]
Dai, W. J. [1 ]
Liu, J. H. [1 ]
Zheng, S. J. [1 ]
机构
[1] Three Gorges Univ, Renhe Hosp, Cardiovasc Internal Dept, Yichang, Hubei, Peoples R China
关键词
beta; 2-AR; Mononuclear cell; Atherosclerosis; Stress; CORONARY HEART-DISEASE; BETA-BLOCKERS; MYOCARDIAL-INFARCTION; RISK; STRESS; WOMEN;
D O I
10.4238/2014.October.7.2
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
The aim of this study was to determine whether monocyte/macrophage beta 2-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 beta 2-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 beta 2-AR, affecting MCP-1 secretion, CCR2 protein expression and cell migration capacity of THP-1 cells. Therefore, monocyte-macrophage beta 2-AR may act as a target of antisympathetic excitation-induced atherosclerotic progression.
引用
收藏
页码:8080 / 8088
页数:9
相关论文
共 20 条
[1]
β-Blocker Use and Clinical Outcomes in Stable Outpatients With and Without Coronary Artery Disease [J].
Bangalore, Sripal ;
Steg, Ph Gabriel ;
Deedwania, Prakash ;
Crowley, Kevin ;
Eagle, Kim A. ;
Goto, Shinya ;
Ohman, E. Magnus ;
Cannon, Christopher P. ;
Smith, Sidney C., Jr. ;
Zeymer, Uwe ;
Hoffman, Elaine B. ;
Messerli, Franz H. ;
Bhatt, Deepak L. .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 2012, 308 (13) :1340-1349
[2]
Stress, inflammation and cardiovascular disease [J].
Black, PH ;
Garbutt, LD .
JOURNAL OF PSYCHOSOMATIC RESEARCH, 2002, 52 (01) :1-23
[3]
CAMEJO G, 1991, CIRCULATION, V84, P17
[4]
CRUICKSHANK JM, 1990, CIRCULATION, V82, P60
[5]
Social and contextual etiology of coronary heart disease in women [J].
Fleury, J ;
Keller, C ;
Murdaugh, C .
JOURNAL OF WOMENS HEALTH & GENDER-BASED MEDICINE, 2000, 9 (09) :967-978
[6]
Genetic polymorphism of beta-adrenergic receptors and mortality in ischemic heart disease [J].
Jaillon, Patrice ;
Simon, Tabassome .
THERAPIE, 2007, 62 (01) :1-7
[7]
β2-Adrenergic receptor genotype and survival among patients receiving β-blocker therapy after an acute coronary syndrome [J].
Lanfear, DE ;
Jones, PG ;
Marsh, S ;
Cresci, S ;
McLeod, HL ;
Spertus, JA .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 2005, 294 (12) :1526-1533
[8]
Madden KS, 2003, BRAIN BEHAV IMMUN, V17, pS5
[9]
Marital stress worsens prognosis in women with coronary heart disease -: The Stockholm Female Coronary Risk Study [J].
Orth-Gomér, K ;
Wamala, SP ;
Horsten, M ;
Schenck-Gustafsson, K ;
Schneiderman, N ;
Mittleman, MA .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 2000, 284 (23) :3008-3014
[10]
Effects of physical and psychological stressors on behavior, macrophage activity, and Ehrlich tumor growth [J].
Palermo-Neto, J ;
Massoco, CD ;
de Souza, WR .
BRAIN BEHAVIOR AND IMMUNITY, 2003, 17 (01) :43-54