The number and function of circulating endothelial progenitor cells in patients with Kawasaki disease

Abstract

Kawasaki disease (KD) is associated with coronary artery injury. Studies have shown that the endothelial progenitor cell (EPC) participates in the process of arterial repair. Data have been reported that the number of EPC increased significantly in the subacute phase of KD. However, until now, there are no data about the functions of EPC in KD patients. The present study was designed to further investigate the number and functions of EPC in KD. Ten KD patients in the acute phase and ten healthy volunteers were recruited and attributed to the KD group and control group, respectively. The circulating CD34/kinase insert domain-containing receptor double positive cells were evaluated in the two groups using flow cytometry. In vitro assays were used to measure the functions of EPC, including proliferation, adhesion, and migration activities. The plasma levels of nitric oxide (NO), tumor necrosis factor-alpha (TNF-alpha), and high sensitivity C-reactive protein (hs-CRP) were also assessed in both groups. The number of EPC in the KD group was significantly higher than that of the control group (0.021 +/- 0.007% vs. 0.014 +/- 0.003%, P < 0.05). The migratory response of EPC was significantly decreased in the KD group, compared with that of the control group (5.50 +/- 1.78 vs. 3.40 +/- 1.35 cells/high power field, P < 0.01). Similarly, the proliferative and adhesive activities of EPC in the KD group were also decreased (0.47 +/- 0.08 vs. 0.66 +/- 0.07, P < 0.01; 6.5 +/- 2.12 vs. 11.2 +/- 2.04 cells/high power field, P < 0.01). The plasma NO, TNF-alpha, and hs-CRP levels in the KD group were higher than those of the control group (54.10 +/- 11.78 vs. 38.80 +/- 11.10 mumol/l, P < 0.01; 48.20 +/- 7.42 vs. 37.00 +/- 11.12 pg/ml, P < 0.05; 87.10 +/- 30.18 vs. 5.30 +/- 3.37 mg/l, P < 0.01). The number of circulating EPC positively correlated with the level of NO (r = 0.92, P < 0.001), and the functions of EPC negatively correlated with the levels of TNF-alpha and hs-CRP, respectively. In Kawasaki disease, the number of EPC was enhanced and the functions of EPC were attenuated. The two-way regulation of circulating EPC in KD patients may be associated with the disorders of cytokines or messengers in KD patients.

Liver X Receptor Agonist Alleviated High Glucose‐Induced Endothelial Progenitor Cell Dysfunction via Inhibition of Reactive Oxygen Species and Activation of AMP‐Activated Protein Kinase

“…Endothelial progenitor cells are early precursors of mature endothelial cells that replenish aging, damaged endothelial cells and rescued endothelial dysfunction [6,20–22]. Endothelial dysfunction is an early marker of atherosclerosis and has been considered as a key factor in the process by initiating and potentiating the development of peripheral and coronary atherosclerotic disease [4,14,25,26].…”

Nitric Oxide-Mediated Coronary Flow Regulation in Patients with Coronary Artery Disease: Recent Advances

“…The number of EPCs was higher, the migratory response of EPCs was decreased, and the proliferative and adhesive activities were decreased in patients with Kawasaki disease compared with those in controls: the plasma NO, tumor necrosis factor-a (TNF-a), and high sensitivity CRP levels in the Kawasaki disease group were higher. 74 The number of circulating EPCs positively correlated with the level of NO, and the functions of EPCs negatively correlated with the levels of TNF-a and CRP. The two-way regulation of circulating EPCs (an increase in the number and a decrease in the function) in Kawasaki disease patients may be associated with the disorders of cytokines or messengers in these patients.…”

Markers of Vascular Damage and Repair

“…EPCs were also measured in other subgroups of vasculitis. In Behcet's vasculitis EPC were decreased 89 , in children with Kawasaki disease EPC were increased 90 . What make these studies so difficult to compare is, again, the lack of standardisation and the use of different assays and surface markers.…”