Serum levels of the MCP-1 chemokine in patients with ischemic stroke and myocardial infarction

被引:128
作者
Arakelyan, A
Petrkova, J
Hermanova, Z
Boyajyan, A
Lukl, J
Petrek, M [1 ]
机构
[1] Palacky Univ, Dept Immunol, Olomouc 77520, Czech Republic
[2] Natl Acad Sci Armenia, Inst Mol Biol, Yerevan, Armenia
[3] Palacky Univ, Dept Internal Med 1, Olomouc 77520, Czech Republic
[4] Fac Hosp Olomouc, Olomouc 77520, Czech Republic
关键词
D O I
10.1155/MI.2005.175
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Chemokine-driven migration of inflammatory cells has been implicated in pathogenesis of atherosclerosis-associated conditions such as ischemic stroke and myocardial infarction. In this study, a candidate chemokine, monocyte chemoattractant protein (MCP)-1, was investigated in patients with both aforementioned manifestations of atheroslerotic inflammation. MCP-1 levels in serum were determined by ELISA in 40 healthy, control subjects (C), 40 patients with ischemic stroke (IS), and in 64 patients with myocardial infarction (MI). Statistical analysis utilised Mann-Whitney test, Fisher's exact test, and Spearman's rank correlation (P <.05). In comparison to control subjects (Q median/interquartile range: 239/126 pg/mL), MCP-1 serum levels were increased in both investigated patient cohorts (IS: 384/370, P <.001; MI: 360/200, P <.002). There was a substantial variability of MCP-1 serum levels, especially in the IS group. No relationship was observed between chemokine levels and atherosclerosis risk factors (hypertension, diabetes, smoking, and alcohol consumption), and MCP-1 was also not related to age or gender. Elevation of MCP-1 in circulation of patients with atherosclerosis-associated complications implicates this CC chemokine ligand (CCL)2 in inflammatory processes, which contribute to pathogenesis of myocardial infarction and ischemic stroke. Further investigations, including patient stratification, are however necessary to evaluate if MCP-1 can be utilised for clinical management of patients with these diseases.
引用
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页码:175 / 179
页数:5
相关论文
共 33 条
[1]   EXPRESSION OF INTERCELLULAR-ADHESION MOLECULE-1 ON RAT CARDIAC MYOCYTES BY MONOCYTE CHEMOATTRACTANT PROTEIN-1 [J].
BAN, K ;
IKEDA, U ;
TAKAHASHI, M ;
KANBE, T ;
KASAHARA, T ;
SHIMADA, K .
CARDIOVASCULAR RESEARCH, 1994, 28 (08) :1258-1262
[2]   Inflammatory bio-markers and cardiovascular risk prediction [J].
Blake, GJ ;
Ridker, PM .
JOURNAL OF INTERNAL MEDICINE, 2002, 252 (04) :283-294
[3]   Association between plasma levels of monocyte chemoattractant protein-1 and long-term clinical outcomes in patients with acute coronary syndromes [J].
de Lemos, JA ;
Morrow, DA ;
Sabatine, MS ;
Murphy, SA ;
Gibson, CM ;
Antman, EM ;
McCabe, CH ;
Cannon, CP ;
Braunwald, E .
CIRCULATION, 2003, 107 (05) :690-695
[4]   Oxidized LDL-mediated monocyte adhesion to endothelial cells does not involve NFκB [J].
Dwivedi, A ;
Änggård, EE ;
Carrier, MJ .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2001, 284 (01) :239-244
[5]   The inflammatory response in myocardial infarction [J].
Frangogiannis, NG ;
Smith, CW ;
Entman, ML .
CARDIOVASCULAR RESEARCH, 2002, 53 (01) :31-47
[6]   The association of leukocyte count, fibrinogen and C-reactive protein with vascular risk factors and ischemic vascular diseases [J].
Grau, AJ ;
Buggle, F ;
Becher, H ;
Werle, E ;
Hacke, W .
THROMBOSIS RESEARCH, 1996, 82 (03) :245-255
[7]  
Gu L, 1999, Chem Immunol, V72, P7, DOI 10.1159/000058723
[8]   Monocyte chemoattractant protein-1 deficiency is protective in a murine stroke model [J].
Hughes, PM ;
Allegrini, PR ;
Rudin, M ;
Perry, VH ;
Mir, AK ;
Wiessner, C .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 2002, 22 (03) :308-317
[9]   Pioglitazone, a peroxisome proliferator-activated receptor-γ agonist, attenuates myocardial ischernia/reperfusion injury in a rat model [J].
Ito, H ;
Nakano, A ;
Kinoshita, M ;
Matsumori, A .
LABORATORY INVESTIGATION, 2003, 83 (12) :1715-1721
[10]   Targeted deletion of CC chemokine receptor 2 attenuates left ventricular remodeling after experimental myocardial infarction [J].
Kaikita, K ;
Hayasaki, T ;
Okuma, T ;
Kuziel, WA ;
Ogawa, H ;
Takeya, M .
AMERICAN JOURNAL OF PATHOLOGY, 2004, 165 (02) :439-447