Reduced number and impaired function of circulating endothelial progenitor cells in patients with abdominal aortic aneurysm

Division of Cardiology, Department of Internal Medicine, Taipei Veterans General Hospital, Taipei, Taiwan
International journal of cardiology (Impact Factor: 4.04). 11/2012; 168(2). DOI: 10.1016/j.ijcard.2012.11.002
Source: PubMed


Circulating endothelial progenitor cells (EPCs) are associated with coronary artery disease (CAD) and predict its outcome. Although the pathophysiology of abdominal aortic aneurysm (AAA) is different, it shares some risk factors with CAD. Therefore, the correlation between EPCs and AAA was investigated.

Methods and results:
Seventy-eight subjects (age 77.2 ± 7.8 years) with suspected AAA were prospectively enrolled. Cut-off values (men, 3.5-5.5 cm; women, 3-5 cm) were used to define normal aorta, small AAA, and large AAA on thoraco-abdominal computer tomography. Endothelial function was measured by flow-mediated vasodilation (FMD). Flow cytometry and colony-forming units (CFUs) were used to evaluate circulating EPC numbers. Circulating EPCs were defined as mononuclear cells with low CD45 staining and double-positive staining for KDR, CD34, or CD133. Late out-growth EPCs were cultured from six patients with large AAAs and six age- and sex-matched controls to evaluate proliferation, adhesion, migration, tube formation, and senescence. FMD was significantly lower with large (5.26% ± 3.11%) and small AAAs (6.31% ± 3.66%) than in controls (8.88% ± 4.83%, P=0.008). Both CFUs (normal 38.39 ± 12.99, small AAA 21.22 ± 7.14, large AAA 6.98 ± 1.97; P=0.026) and circulating EPCs (CD34(+)/KDR(+) and CD133(+)/KDR(+)) were significantly fewer in AAA patients than in controls. On multivariate analysis, CFUs and circulating EPCs (CD34(+)/KDR(+)) were independently, inversely correlated to AAA diameter. Proliferation, adhesion, migration, tube formation, and senescence of late EPCs were significantly impaired in AAA patients.

The number and function of EPCs were impaired in AAA patients, suggesting their potential role in AAA.

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Available from: Yung-Hsiang Chen,
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    • "Endothelial dysfunction has been associated with decreased circulating endothelial progenitor cells (1,2) and increased circulating endothelial microparticles (3,4). Both conditions are influenced by classic risk factors (4-6) and inflammatory status (7,8). "
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    ABSTRACT: It is not known whether the addition of ezetimibe to statins adds cardiovascular protection beyond the expected changes in lipid levels. Subjects with coronary heart disease were treated with four consecutive 1-week courses of therapy (T) and evaluations. The courses were: T1, 100 mg aspirin alone; T2, 100 mg aspirin and 40 mg simvastatin/10 mg ezetimibe; T3, 40 mg simvastatin/10 mg ezetimibe, and 75 mg clopidogrel (300 mg initial loading dose); T4, 75 mg clopidogrel alone. Platelet aggregation was examined in whole blood. Endothelial microparticles (CD51), platelet microparticles (CD42/CD31), and endothelial progenitor cells (CD34/CD133; CDKDR/CD133, or CD34/KDR) were quantified by flow cytometry. Endothelial function was examined by flow-mediated dilation. Comparisons between therapies revealed differences in lipids (T2 and T3<T1 and T4 for total cholesterol, LDL-C, and triglycerides; P<0.002 for all), as well as for endothelial function (T2>T1 and T4, P=0.001). Decreased platelet aggregation was observed after aspirin (arachidonic acid, T1<T3 and T4, P=0.034) and clopidogrel (adenosine, T3 and T4<T1 and T2, P<0.0001) therapy. Simvastatin/ezetimibe diphosphate did not change platelet aggregation, the amount of circulating endothelial and platelet microparticles, or endothelial progenitor cells. Cardiovascular protection following therapy with simvastatin/ezetimibe seems restricted to lipid changes and improvement of endothelial function not affecting the release of microparticles, mobilization of endothelial progenitor cells or decreased platelet aggregation.
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    • "Previous vascular repairing and regeneration studies using EPCs usually focused on coronary and peripheral vasculature injury. They showed a precise treatment efficacy and many prospective applications[9], [10], [11], [12], [13], [14], [15]. Recently, growing studies have confirmed that EPCs, as an important factor in the process of systemic vascular protection and restoration, play a critical role in endothelial maintenance, the vascular repairing process, and postnatal vasculogenesis[16], [17], [18]. "
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    ABSTRACT: Aneurysm embolization with coil is now widely used clinically. However, the recurrence of aneurysms after embolization has always plagued neurosurgeons because the endothelial layer of the aneurysm neck loses its integrity after being embolized by coil. Bone marrow-derived endothelial progenitor cells (BM-EPCs) could be incorporated into injured endothelium and differentiate into mature endothelial cells during vascular repairing processes. The aim of our study is to explore the effects of BM-EPCs on aneurysm repairing and remodeling in a rat embolization model of abdominal aortic aneurysm. BM-EPC proliferation, migration and tube formation were not affected by super-paramagnetic iron oxide nanoparticle (SPIO) labeling compared to the controls (p>0.05). The number of SPIO-labeled cells greatly increased in EPC transplanted rats compared to that of phosphate buffered saline treated rats. SPIO-labeled EPC (SPIO-EPC) are mainly located in the aneurysm neck and surrounded by fibrous tissue. A histology study showed that the aneurysm orifice was closed with neointima and the aneurysm was filled with newly formed fibrous tissue. The SPIO-EPC accumulated in the aneurysm neck, which accelerated focal fibrous tissue remodeling, suggesting that BM-EPCs play a crucial role in repairing and remodeling the aneurysm neck orifice.
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