Circulating Endothelial Progenitor Cells as a New Marker of Endothelial Dysfunction or Repair in Acute Stroke

Circulating bone marrow (BM)-derived stem and progenitor cells (SPCs) participate in turnover of vascular endothelium and myocardial repair after acute coronary syndromes. Acute myocardial infarction (MI) produces a generalized inflammatory reaction, including mobilization of SPCs, increased local production of chemoattractants in the ischemic myocardium, as well as neural and humoral signals activating the SPC egress from the BM. Several types of circulating BM cells were identified in the peripheral blood, including hematopoietic stem cells, endothelial progenitor cells, mesenchymal stromal cells, circulating angiogenic cells and pluripotent very small embryonic-like cells; however, the contribution of circulating cells to the myocardial and endothelial repair is still unknown. The number and function of these cells is impaired in patients with diabetes and other cardiovascular risk factors, but can be improved by physical exercise and use of statins. The mobilization of SPCs in acute coronary syndromes and stable coronary artery disease seems to predict the clinical outcomes in selected groups of patients. Interpretation of the findings has to incorporate other factors that modulate the process of mobilization, such as coexisting diseases, age and medications. This review discusses the mobilization of SPCs in acute ischemia (MI, stroke), as well as in stable cardiovascular disease, and highlights the possibility of using the SPC as a marker of cardiovascular risk.

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“…The number of cells was measured, however, B1 week after the stroke, which might be too late to measure the 'true' reparative cells. 32 …”

Section: Strokementioning

confidence: 99%

Mobilization of stem and progenitor cells in cardiovascular diseases

et al. 2011

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“…Colonies were counted manually in a minimum of 3 wells in 12-well plates by two independent observers who were unaware of clinical profiles; results are expressed as average number of CFUs per well. In selected samples, the endothelial phenotype was confirmed using specific indicators, that is, according to the uptake of 1,1 0 -dioctadecyl-3,3,3 0 ,3 0 -tetramethylindocarbocyanine-labeled acetylated low-density lipoprotein (Biomedical Technologies Inc., Stoughton, MA, USA), and by immunostaining using FITC-labeled Ulex europaeus agglutinin-1 (Sigma) and anti-CD31 (1:20; DAKO, Carpinteria, CA, USA), antivascular endothelium cadherin (1:50; Chemicon, Billerica, MA, USA), anti-CD34 (1:20; DAKO), and anti-kinase domain receptor (1:50; Sigma) antibodies, as previously described (Hur et al, 2004;Yoon et al, 2005;Chu et al, 2008;Jung et al, 2008).…”

Section: Colony-forming Unit Countsmentioning

confidence: 99%

“…Furthermore, it was recently suggested that reduced numbers and impaired functions of circulating EPCs are related to the pathogenesis of stroke (Ghani et al, 2005;Chu et al, 2008). Thus, given that MMD involves dynamic interplay between arterial occlusion and neovascularization, the involvement of EPCs in MMD may be more complex than in other cerebrovascular occlusive diseases.…”

Section: Introductionmentioning

confidence: 99%

Circulating Endothelial Progenitor Cells as a Pathogenetic Marker of Moyamoya Disease

Jung

Chu

Park

et al. 2008

J Cereb Blood Flow Metab

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Moyamoya disease (MMD) is an unusual form of chronic cerebrovascular occlusive disease that involves the formation of characteristically abnormal vessels. Recent studies have reported that colony-forming unit (CFU) and outgrowth cells represent a subpopulation of endothelial progenitor cells (EPCs). Here, we attempted to determine the significance of CFU number and outgrowth cell yield in MMD. Endothelial progenitor cells were isolated from the blood of 24 adult MMD patients and from 48 age-and risk factor-matched control subjects. After 7 days of culture, CFUs were determined, and yields of outgrowth cells were measured during 2 months of culture. The EPC function was also evaluated using matrigel plate assays. It was found that CFU numbers were significantly lower in MMD patients than in controls. Moreover, during long-term culture, outgrowth cells were isolated from only 10% of control subjects but from 33% of MMD patients, and CFU numbers and tube formation were found to be lower in advanced MMD cases than in those with early stage disease, whereas outgrowth cells were more frequently detected in those with early MMD and moyamoya vessels than in those with advanced disease. These characteristics of circulating EPCs reflect mixed conditions of vascular occlusion and abnormal vasculogenesis during the pathogenesis of MMD.

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“…On the positive side, in animal studies, EPCs have been shown to participate in the formation of new vessels and to increase blood flow in ischemic areas. 25 Increased levels of circulating EPCs and reduced ischemic damage were found after diabetic mice with middle cerebral artery occlusion were infused with EPCs preincubated with wildtype membrane microparticles. 18 EPC numbers can be increased by exercise and with ACE inhibitors and receptor blockers, statins, and erythropoietin.…”

mentioning

confidence: 99%

“…These immature endothelial cell-derived bone marrow stem cells circulate in peripheral blood. 24,25 Endothelial injury appears to act as a trigger for these cells in the repair of damaged endothelial cells. Such a potential "miracle cure" has both benefits and risks.…”

mentioning

confidence: 99%

Role of the vascular endothelium and plaque in acute ischemic stroke

Madden

2012

Neurology

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The underlying cause of stroke lies in the damage to the arterial endothelial cell layer. The most profound damage is due to atherosclerosis, which can either occlude an artery or produce a thromboembolism. Diabetes and inflammation contribute to atherosclerosis and the associated endothelial damage by initiating and promoting the deposition of modified lipids in the subendothelium and by inhibiting endothelial nitric oxide (NO) production. At the same time, both production of endothelin-1 and generation of reactive oxygen species increase. In addition, leukocytes adhere to the endothelium and levels of C-reactive protein increase. The stroke that ensues upon cerebral artery occlusion or plaque rupture continues and exacerbates endothelial damage. Statins have been shown to be helpful in preventing stroke and diminishing its consequences. An international clinical trial to determine if an NO donor is effective (Efficacy of Nitric Oxide in Stroke study) is currently under way. Other interventions such as antioxidants, kinase inhibition, and endothelial progenitor cells offer promising avenues of research and perhaps therapeutic avenues for treatment of stroke. This article discusses the role of the vascular endothelium in ischemic stroke and those interventions that may provide plausible avenues for future therapy. Neurology GLOSSARYBMSCs ϭ bone marrow stromal cells; CRP ϭ C-reactive protein; EDHF ϭ endothelium-derived hyperpolarizing factor; eNOS ϭ endothelial nitric oxide synthase; EPC ϭ endothelial progenitor cell; ET ϭ endothelin; HT ϭ hemorrhagic transformation; MMPs ϭ matrix metalloproteases; NO ϭ nitric oxide; RAAS ϭ renin-angiotensin-aldosterone system; ROS ϭ reactive oxygen species.

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Circulating Endothelial Progenitor Cells as a New Marker of Endothelial Dysfunction or Repair in Acute Stroke

Cited by 108 publications

References 34 publications

Mobilization of stem and progenitor cells in cardiovascular diseases

Mobilization of stem and progenitor cells in cardiovascular diseases

Circulating Endothelial Progenitor Cells as a Pathogenetic Marker of Moyamoya Disease

Role of the vascular endothelium and plaque in acute ischemic stroke

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