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ABSTRACT: Data have shown that circulating endothelial progenitor cells (EPCs) closely correlate with the vascular endothelial layer state. The present study was designed to describe the evolution of EPCs in children before and 24 h after transcatheter closure surgery for occluding congenital heart disease. Three groups of patients were studied: the transcatheter closure of atrial septal defect (ASD) group (group 1), the transcatheter closure of patent ductus arteriosus (PDA) group (group 2), and the transcatheter closure of ventricular septal defect (VSD) group (group 3). The circulating EPC level was detected using flow cytometry measuring CD34 and kinase insert receptor double-positive mononuclear cells. The concentration of vascular endothelial growth factor (VEGF) was assessed by enzyme-linked immunosorbent assay. The fluoroscopy time was correctly recorded during the surgery. All of the data were collected before and 24 h after surgery. EPC level and VEGF concentration did not change significantly before and at 24 h after surgery in groups 1 and 2. In group 3, the level of circulating EPCs and VEGF concentration increased significantly 24 h after surgery. The fluoroscopy time in group 3 was significantly longer than in groups 1 and 2. The increased volume of EPCs and VEGF were positively correlated in group 3. Our results showed that transcatheter closure of PDA and ASD in children does not lead to increased circulating level of EPCs. Transcatheter closure of VSD may result in vascular endothelium injury as indicated by increased circulating EPC level.
Pediatric Cardiology 02/2013; · 1.30 Impact Factor
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ABSTRACT: To study the effects of intravenous immunoglobulin (IVIG) and aspirin treatment on the functions of circulating endothelial progenitor cells (EPCs) in children with Kawasaki disease (KD) and possible mechanisms.
Blood samples were obtained in 10 children with KD before and 7 days after the treatment by IVIG and aspirin. MTT method, modified Boyden chamber method and cell culture plate adhesion method were used to assess the functions of EPCs, including proliferation, adhension and migration activities. The plasma levels of tumor necrosis factor-α (TNF-α) and high-sensitivity C reactive protein (hs-CRP) were also measured.
The functions of circulating EPCs 7 days after IVIG and aspirin treatment were significantly improved. IVIG and aspirin treatment significantly reduced plasma TNF-α and hs-CRP concentrations. There was a significant linear regression relationship between the reduced plasma TNF-α and hs-CRP levels and the increased functions of circulating EPCs.
IVIG and aspirin treatment can improve the functions of circulating EPCs, possibly through reducing plasma concentrations of TNF-α and hs-CRP.
Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics 12/2011; 13(12):966-9.
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ABSTRACT: We sought to determine the effects of treatment with intravenous immunoglobulin (IVIG) and aspirin on the functions of endothelial progenitor cells (EPCs) in patients with Kawasaki disease (KD) as well as its relationship with concentrations of tumor necrosis factor-α (TNF-α) and high-sensitivity C-reactive protein (hs-CRP). Ten KD patients in the acute phase of their disease were recruited. We investigated EPC functions in children with KD before and after treatment with IVIG and aspirin. In vitro assays were used to measure the functions, including proliferation, adhesion, and migration activities, of EPCs. Plasma levels of TNF-α and hs-CRP were also assessed. All of the data were assessed before and at 7 days after treatment initiation. EPC functions after 7 days of treatment with IVIG and aspirin were significantly improved than they were before treatment with IVIG and aspirin. Treatment with IVIG and aspirin significantly decreased TNF-α and hs-CRP concentrations. There was a significant linear regression relationship between decreased plasma TNF-α levels, hs-CRP levels, and increased functions of circulating EPCs. The results of our study indicate that the functions of circulating EPCs improved after treatment with IVIG and aspirin, which may be related to decreased concentrations of TNF-α and hs-CRP.
Pediatric Cardiology 02/2011; 32(4):455-60. · 1.30 Impact Factor
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Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics 10/2010; 12(10):825-6.
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ABSTRACT: To study the function of circulating endothelial progenitor cells and its relationship with serum concentrations of high-sensitivity C-reactive protein (Hs-CRP) in children with Kawasaki disease.
Ten children with Kawasaki disease and ten healthy children as a control group were enrolled. The peripheral mononuclear cells were induced into endothelial progenitor cells using Dulbecco's Modified Eagle Medium containing vascular endothelial growth factor and basic fibroblast growth factor. The proliferative ability, migratory ability and adhesive ability of endothelial progenitor cells were assessed by MTT methods, modified Boyden chamber methods and cell culture plate adhesion method, respectively. The concentrations of serum Hs-CRP were measured by latex enhanced turbidimetric immunoassay.
The proliferative ability, migratory ability and adhesive ability of endothelial progenitor cells in the Kawasaki disease group were significantly lower than those in the control group (P<0.01). The serum concentrations of Hs-CRP in the Kawasaki disease group were significantly higher than those in the control group (87.1+/-30.2 mg/L vs 5.3+/-3.4 mg/L; P<0.01). The function of circulating endothelial progenitor cells was negatively correlated with serum concentrations of Hs-CRP in the Kawasaki disease group.
The function of circulating endothelial progenitor cells is decreased in children with Kawasaki disease, which may be associated with the abnormal expression of inflammatory mediators.
Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics 07/2010; 12(7):513-7.
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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.
European Journal of Pediatrics 06/2009; 169(3):289-96. · 1.88 Impact Factor
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ABSTRACT: Elevated circulating endothelial microparticles (EMPs) are associated with endothelial dysfunction. This study is to investigate whether berberine-induced fall in circulating EMPs facilitates improvement of endothelial function in healthy subjects. Fourteen healthy subjects received 1-month berberine therapy (1.2 g/d) and 11 healthy subjects served as control. Circulating EMPs were measured by flow cytometric analysis before and after therapy. Brachial artery endothelium-dependent and -independent function was assessed by flow-mediated vasodilation (FMD) and sublinqual nitroglyceride-mediated vasodilation (NMD). In vitro, human umbilical vein endothelial cells (HUVECs) were stimulated by EMPs (10(6)/ml) with or without the presence of berberine (10 microM). Intracellular endothelial nitric oxide synthase (eNOS) protein expression was detected by flow cytometry. After berberine therapy, circulating CD31(+)/CD42(-) microparticles were reduced, which was in parallel with the improvement of flow-mediated vasodilation while nitroglyceride-mediated vasodilation kept unchanged. A robust relationship was found between drop of circulating CD31(+)/CD42(-) microparticles and increased flow-mediated vasodilation. The EMPs in vitro led to diminished eNOS protein expression in HUVECs and this EMP-mediated detrimental effect was markedly inhibited by berberine. Berberine-induced decline in circulating CD31(+)/CD42(-) microparticles contributes to upregulation of endothelial function in healthy subjects. Deceasing EMPs may be a novel therapeutic target for the improvement of endothelial dysfunction in humans.
European journal of pharmacology 05/2009; 614(1-3):77-83. · 2.59 Impact Factor
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ABSTRACT: Berberine (BR) has a beneficial effect on endothelial function by increasing nitric oxide (NO), as NO plays a pivotal role in the regulation of endothelial progenitor cell (EPC) mobilization and function. The aim of the present study was to investigate whether BR-induced upregulation of circulating EPCs is related to NO production in healthy subjects.
Twenty volunteers were recruited and received 400 mg of BR 3 times a day for 30 days. We assessed the number of EPC colony-forming units (EPC-CFUs), as well as the proliferative, adhesive and migratory activities of circulating EPCs before and after the 30-day BR therapy. The level of plasma NO was also measured before and after the 30-day BR therapy.
After 30 days of BR therapy, the number of EPC-CFUs was increased and the function of EPCs, including proliferation, adhesion and migration, was augmented. In parallel, BR therapy enhanced the plasma NO level. There was a significant linear regression relationship between the enhanced plasma NO level and the increased number and function of circulating EPCs.
BR-induced upregulation of the number and function of circulating EPCs in healthy subjects is related to NO production.
Cardiology 10/2008; 112(4):279-86. · 1.71 Impact Factor
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ABSTRACT: Impaired artery elasticity has been found in various pathological conditions related to endothelial dysfunction. Recently, CD31+/CD42- microparticles (MPs) emerged as a marker of endothelial injury. Whether CD31+/CD42- MPs, generated under physiological conditions, are correlated with artery properties has not been reported.
We evaluated brachia-ankle pulse-wave velocity (baPWV) (n = 76) and C1 large-artery and C2 small-artery elasticity indices (n = 56), using noninvasive devices for pulse-wave analysis in a group of healthy persons. The number of circulating CD31+/CD427- MPs (n = 76) was measured by flow cytometric analysis.
Circulating CD31+/CD42- MPs were positively correlated with values of baPWV (r = 0.371, P = .008) and with C1 large-artery and C2 small-artery elasticity indices (r = -0.294, P = .037; and r = -0.310, P = .027, respectively). Multivariate analysis identified CD31+/CD42- MPs as potent contributors to the development of impaired systemic artery elasticity.
The level of circulating CD31+/CD42- MPs, an important biomarker of dysfunctional endothelium and vascular injury, is closely associated with impaired systemic artery elasticity in healthy subjects. The present study suggests that CD31+/CD42- MPs may be a novel surrogate marker for the clinical evaluation of vascular damage.
American Journal of Hypertension 10/2007; 20(9):957-64. · 3.18 Impact Factor
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ABSTRACT: To observe the effect of fluid shear stress on the eNOS gene expression and NO production in endothelial progenitor cells (EPCs).
The peripheral blood mononuclear cells from healthy volunteers were inducted into EPCs and divided into stationary group (0 dyn/cm(2), 1 dyn/cm(2) = 0.1 Pa), low-flow shear stress group (5 dyn/cm(2)), medium-flow shear stress group (15 dyn/cm(2)) and high-flow shear stress group (25 dyn/cm(2)). The effects of shear stress on the endothelial nitric oxide synthase (eNOS) gene expression and nitric oxide (NO) production in human EPCs were measured.
Typical "spindle-shaped" appearance was shown in EPCs derived from peripheral blood mononuclear cells and were positively labeled by acetylated-LDL, lectin, FLK-1 and vWF. After 4 hours treatment with various shear stresses, the ratio of eNOS/beta-actin mRNA expression by human EPCs in low, medium and high-flow shear stress group was 0.364, 0.505 and 0.548 respectively, which was significantly higher than that in stationary group (0.183, all P < 0.05) and the NO secretion in human EPCs in low, medium and high-flow shear stress group was also significantly higher than that in stationary group (all P < 0.05).
Fluid shear stress enhances the eNOS mRNA expression and NO secretion in human EPCs, therefore, shear stress could potentiate the repair efficacy of EPCs for endothelial injury.
Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] 05/2007; 35(4):359-62.
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ABSTRACT: Pulse wave velocity and flow-mediated vasodilation (FMD) are widely used as noninvasive modalities for evaluating atherosclerosis. However, it is not known whether pulse wave velocity is related to FMD in patients with coronary artery disease (CAD). Therefore, the present study was designed to investigate the alteration in brachial-ankle pulse wave velocity (baPWV) and endothelial function in CAD patients.
Thirty-three patients with CAD and thirty control subjects were recruited for this study. baPWV was measured non-invasively using a VP 1000 automated PWV/ABI analyzer (PWV/ABI, Colin Co. Ltd., Komaki, Japan). Endothelial function as reflected by FMD in the brachial artery was assessed with a high-resolution ultrasound device.
baPWV was increased in CAD patients compared with control subjects [(1756.1 +/- 253.1) cm/s vs (1495.3 +/- 202.3) cm/s, P < 0.01]. FMD was significantly reduced in CAD patients compared with control subjects [(5.2 +/- 2.1)% vs (11.1 +/- 4.4)%, P < 0.01]. baPWV correlated with FMD (r = -0.68, P < 0.001). The endothelium-independent vasodilation induced by sublingual nitroglycerin in the brachial artery was similar in the CAD group compared with the control group.
CAD is associated with increased baPWV and endothelial dysfunction. Increased baPWV parallels diminished endothelial function. Our data therefore suggest that baPWV can be used as a noninvasive surrogate index in clinical evaluation of endothelial function.
Chinese medical journal 11/2006; 119(22):1866-70. · 0.86 Impact Factor
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ABSTRACT: Seeding endothelial progenitor cells (EPCs) onto the surface of vascular grafts has been proved to be a promising strategy to improve nonthrombogenic potentials of small diameter artificial vessels. Here, we investigated whether in vitro shear stress modulates the tissue-type plasminogen activator (t-PA) secretion and mRNA expression in human EPCs and improves patency of the EPC-seeded polyurethane small diameter vascular grafts implanted in the canine carotid artery in vivo. In vitro shear stress, in a dose-dependent manner, increased t-PA secretion and mRNA expression of human EPCs. The in vivo implantation of EPC-seeded vascular grafts remained highly patent in shear stress pretreatment compared with stationary condition. The present findings demonstrate for the first time that in vitro shear stress can enhance t-PA secretion and gene expression in human EPCs, which contributes to improvement in nonthrombogenic potentials of EPC-seeded small diameter artificial vessels with maintenance of in vivo highly patency rate.
Biochemical and Biophysical Research Communications 05/2006; 342(2):577-84. · 2.48 Impact Factor
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ABSTRACT: The present study was designed to investigate whether Tumor necrosis factor (TNF)-alpha stimulates release of endothelial microparticles (EMPs) by human endothelial cells, and whether EMPs may serve as a promising marker for endothelial injury and dysfunction.
Human umbilical venous endothelial cells (HUVEC) were incubated with or without TNF-alpha for 24 hours at 37 degrees C. EMPs generated on the surface of HUVEC were observed with a scanning electron microscopy. The CD31 and CD51 positive EMPs in culture supernatants were measured by flow cytometer.
Fewer vesicles were observed on cell surface of control group, in TNF-alpha-stimulated one, however, cells manifested a blebby surface (eruption phenomenon) and more vesicles on surface were observed. The levels of EMPs were significantly increased in TNF-alpha stimulated cells compared with controls [CD31 + EMP, (164 +/- 63)/1000 cells vs. (42 +/- 10)/1000 cells, P < 0.05; CD51 + EMP, (260 +/- 108)/1000 cells vs. (19 +/- 4)/1000 cells, P < 0.05].
TNF-alpha can stimulate HUVEC to release EMPs which may serve as a surrogate marker for endothelial injury and dysfunction.
Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] 12/2005; 33(12):1137-40.
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ABSTRACT: To investigate the relationship between endothelial progenitors cells (EPCs) and endothelium-dependent vasodilation in patients with unstable angina pectoris.
Thirty patients with unstable angina pectoris (UAP) and thirty control subjects were recruited. Flow-mediated dilation (FMD) in the brachial artery was evaluated by using ultrasound Doppler flow method. The number of circulating EPCs was analyzed by flow cytometry analysis. Total mononuclear cells were isolated from peripheral blood by Ficoll density gradient centrifugation, and then the cells were plated on fibronectin-coated culture dishes. CD34 antigen of adherent cells was identified by immunohistochemical assay. EPCs were characterized as adherent cells double positive for FITC-UEA-I binding and DiI-acLDL uptake by direct fluorescent staining under inverted fluorescent microscope.
FMD was significantly impaired in the UAP group compared with the control group (5.93% +/- 2.67% vs 11.1% +/- 4.36%, P < 0.05). There was no significant difference in NMD between two groups (13.60% +/- 5.03% vs 14.18% +/- 4.50%, P > 0.05). The number of CD34(+) cells significantly increased in the UAP group compared with the control group (0.13% +/- 0.05% vs 0.09% +/- 0.04%, P < 0.05). There was a negative association between impaired FMD and increased CD34(+) cell (r = -0.385, P < 0.05). A positive antigen of CD34 of adhesion cells and double positive adhesion cells were found.
This study shows that the levels of peripheral CD34(+) cells in patients with UAP increase with an impaired endothelial function. The increase in EPCs may be an important compensatory response to acute coronary ischemia and impaired endothelium in patients with UAP.
Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] 11/2005; 33(11):1014-7.
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ABSTRACT: In order to investigate the role of shear stress in the regulation of endothelial function, we assessed here effects of shear stress on tissue-type plasminogen activator in human endothelial progenitor cells (EPCs).
The peripheral blood mononuclear cells were separated from healthy adult and inducted into EPCs, which were identified by double staining for the fluorescent labeled acetylated-LDL and lectin. EPCs were seeded on the small diameter artificial vessels, and then divided into four different experimental groups including stationary group, low-flow shear stress group (5 dyn/cm(2)), medium-flow shear stress group (15 dyn/cm(2)) and high-flow shear stress group (25 dyn/cm(2)). The levels of t-PA in EPC culture medium at 0 hour, 5 hours, 10 hours, 15 hours, 20 hours and 25 hours after culture were measured by enzyme-linked immunosorbent assay.
The peripheral blood mononuclear cells differentiated into EPCs after induction, which were positively labeled by fluorescent acetylated-LDL and lectin. Shear stress enhanced production of the t-PA by EPCs, which was paralleled to levels and times of shear stress.
Shear stress increases t-PA secretion by human EPCs, suggesting that shear stress not only regulates vascular endothelial function but also participates in the pathogenesis of arteriosclerosis.
Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] 10/2005; 33(9):840-2.
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ABSTRACT: Reduced arterial elasticity is a hallmark of aging in healthy humans independently of diseases and endothelial-cell injury and dysfunction may be responsible for this fall in arterial elasticity. We hypothesized that circulating endothelial progenitor cells (EPCs) are involved in endothelial repair and that lack of EPCs contributes to impaired arterial elasticity.
A total of 56 healthy male volunteers were divided into young (n = 26) and elderly (n = 30) groups. Large and small artery elasticity indices were non-invasively assessed by using pulse wave analysis. Flow cytometer was used to count the number of circulating CD34(+) mononuclear cells (MNCs), which were isolated from peripheral blood by Ficoll density gradient centrifugation, and then the cells were plated on fibronectin-coated culture dishes. EPCs were characterized as adherent cells double positive staining for DiI-acLDL uptake and lectin binding with using fluorescent microscope.
C(1) (large artery elasticity index) and C(2) (small artery elasticity index) were significantly reduced in the elderly group compared with those in the young group (11.73 +/- 1.45 vs 16.89 +/- 1.69 ml/mm Hg x 10, P < 0.001; 8.40 +/- 1.45 vs 10.58 +/- 1.18 ml/mm Hg x 100, P < 0.001 respectively). In parallel, the number of circulating EPCs was significantly reduced in the elderly group compared with the young group (0.13 +/- 0.02 vs 0.17 +/- 0.04%, P < 0.05). The number of circulating EPCs correlated with C(1) large and C(2) small artery elasticity indices (r = 0.47, P < 0.01; r = 0.4, P < 0.01). Fluorescent microscope was used to identify EPCs, which were double positive staining for DiI-acLDL uptake and lectin binding.
The present findings suggested that the fall in circulating EPCs with subsequently impaired endothelial-cell repair and function might contribute to reduced arterial elasticity in humans with aging. The decrease in circulating EPCs could serve as a surrogate biologic measure of vascular function and human age.
Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] 05/2005; 33(4):347-50.
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ABSTRACT: To investigate the change in endothelium-dependent vasodilation and arterial elasticity and the association between them in patients with coronary artery disease (CAD).
Thirty patients with CAD and thirty control subjects were recruited for this study. Flow-mediated dilation (FMD) in the brachial artery was evaluated by ultrasound Doppler flow method. They also underwent a non-invasive assessment of C(1) large artery and C(2) small artery indices by using pulse wave analysis.
FMD was significantly reduced in CAD group compared with that in control group [(5.17 +/- 2.13)% vs (11.1 +/- 4.36)%, P < 0.05], C(1) large artery elasticity index was similar between the two groups [(11.59 +/- 4.56) ml/mm Hg x 10 vs (12.11 +/- 3.82) ml/mm Hg x 10, P > 0.05]. However, C(2) small artery elasticity index was significantly reduced in CAD group compared with that in control group [(4.20 +/- 1.80) ml/mm Hg x 100 vs (6.26 +/- 2.36) ml/mm Hg x 100, P < 0.05]. There was a positive association between reduced C(2) small artery elasticity index and impaired FMD (r = 0.53, P < 0.05).
There were impaired endothelium-dependent vasodilation and reduced C(2) small artery elasticity index in the patients with CAD, which were closely correlated with each other. The present study suggested that the measurement of C(2) small artery elasticity might be used as a novel index for the determination of endothelial function.
Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] 02/2005; 33(2):150-2.
