CXCR3 Chemokine Receptor - Plasma IP10 Interaction in Patients With Coronary Artery Disease
Male
Receptors, CXCR3
Coronary Stenosis
Coronary Artery Disease
Middle Aged
Flow Cytometry
Monocytes
Chemokine CXCL10
Coronary Restenosis
03 medical and health sciences
Sex Factors
0302 clinical medicine
Case-Control Studies
Humans
Female
Receptors, Chemokine
Lymphocytes
Chemokines, CXC
Aged
Protein Binding
Signal Transduction
DOI:
10.1253/circj.67.851
Publication Date:
2003-09-25T06:43:08Z
AUTHORS (10)
ABSTRACT
In rat models of transplant vasculopathy, the strongest staining of CXCR3 is observed in the innermost layer of the neointima and because neointimal hyperplasia is seen after coronary angioplasty, the CXC chemokines may be targets for preventing stenosis. The expression of leukocyte surface chemokine receptors (CCR2/CCR5/CXCR2/CXCR3), as determined by flow cytometry, and plasma concentrations of monocyte chemoattractant protein (MCP)-1 and interferon-inducible protein (IP)10, as determined by enzyme immunoassays, were investigated in 55 patients with coronary artery disease (CAD) who underwent percutaneous transluminal coronary angioplasty (PTCA) and 20 patients without significant coronary stenosis based on the results of coronary catheterization during the same period (C group). The patients with CAD were divided into 3 groups: 20 with de novo stenosis (D group), 15 with restenosis (R group) and 20 without restenosis (N group) after PTCA. CXCR3 expression on lymphocytes, but not monocytes, in the R group was significantly lower than that in the C group. Although the plasma concentrations of IP10 in the D and N groups did not differ from that in the C group, the concentration in the R group was significantly higher. Increased plasma concentrations of IP10 were accompanied by a compensatory decrease in the CXCR3 expression on lymphocytes, but not monocytes, suggesting that a high plasma concentration of IP10 strongly induces monocytes signaling. The CXCR3 - plasma IP10 chemokine receptor - chemokine interaction on monocytes may affect the development of coronary restenosis, but not de novo stenosis, in patients with CAD.
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