Exercise acutely increases circulating endothelial progenitor cells and monocyte-/macrophage-derived angiogenic cells

Rehman, Jalees; Li, Jingling; Parvathaneni, Lakshmi; Karlsson, Gudjon; Panchal, Vipul R.; Temm, Constance J.; Mahenthiran, Jo; March, Keith L.

doi:10.1016/j.jacc.2004.02.049

Cited by 287 publications

(225 citation statements)

References 17 publications

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“…Our protocol can identify CD34À ECs (4) Incorrect gating strategy: Analyzing only CD45À cells leads to the exclusion of possible CD45+ ECs. ECs are evaluated as progenitors, which resemble lymphocytes, and so cells in the lymphocyte region in FS and SS are gated during flow cytometry [26,30]. This approach might cause the exclusion of ECs with different morphologic features, as we saw with our data showing variable EC size and morphology.…”

Section: Discussionmentioning

confidence: 91%

Flow cytometric evaluation of circulating endothelial cells: A new protocol for identifying endothelial cells at several stages of differentiation

et al. 2007

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Several factors may influence the analysis of endothelial cells (ECs) by flow cytometry: separation of mononuclear cell, washing and centrifugation steps, panel of monoclonal antibodies, and the lack of standardization of gating technique. Therefore, the reliable quantification of ECs remains a technical challenge. The purpose of this study is to define a new flow cytometric protocol to characterize and quantitate ECs. In previous investigations, increased numbers of circulating ECs have been found in sickle cell disease. The patients with sickle cell disease might provide useful material for the study. We performed flow cytometry on whole blood from 20 normal controls and 31 patients with sickle cell disease (20 patients with steadystate disease and 11 patients with vaso-occlusive crises) using a lyse/no-wash procedure, specific and nonspecific antibody combinations (CD146, CD144, CD34, and CD117), and broad gating. This protocol produced much higher values for the number of circulating ECs (a mean of 2,396.55 ± 658.37 ECs/mL in controls vs 6,709.60 ± 1,772.32 ECs/mL in the steady-state group, or 18,213.50 ± 8,451 in the vaso-occlusive crises group, P < 0.001 for both), and also showed variable EC size and granularity, which may reflect activated, or early release ECs. This novel protocol performed comparably in terms of reproducibility, reliability, and dilution linearity with a previously described protocol. This approach has significant advantages for the characterization and quantitation ECs compatible with the pathophysiology. Using the specific antibodies, CD146 and CD144, together may give more informative EC data than the general approach used. Am. J. Hematol. 82:706-711, 2007. V

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Section: Discussionmentioning

confidence: 91%

Flow cytometric evaluation of circulating endothelial cells: A new protocol for identifying endothelial cells at several stages of differentiation

et al. 2007

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“…Here we studied circulating EPCs expressing an endothelial marker (VEGFR-2/VE-cadherin) and a haemopoietic stem cell or bone-marrow-derived marker (CD34/CD133), and also circulating progenitor cell subtypes expressing haemopoietic stem cell markers alone (CD34/CD133) [7,[11][12][13][14][15]17]. We found significant reductions in circulating cell counts of some populations of both classes of cells (endothelial progenitor, circulating progenitor cell subtypes) in young people with type 1 diabetes without any macrovascular disease or microalbuminuria.…”

Section: Discussionmentioning

confidence: 99%

“…EPCs are a heterogeneous population characterised by the expression of surface markers of endothelial (vascular endothelial [VE]-cadherin [also known as CD144], vascular endothelial growth factor receptor 2 [VEGFR-2], CD31 and von Willebrand factor) and haemopoietic progenitor (CD34, CD133) lineages [7,[11][12][13][14][15][16]. Circulating EPCs consist of cells at various stages of maturation.…”

Section: Introductionmentioning

confidence: 99%

Circulating endothelial progenitor cells, endothelial function, carotid intima–media thickness and circulating markers of endothelial dysfunction in people with type 1 diabetes without macrovascular disease or microalbuminuria

et al. 2009

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Aims/hypothesis Type 1 diabetes is associated with premature arterial disease. Bone-marrow derived, circulating endothelial progenitor cells (EPCs) are believed to contribute to endothelial repair. The hypothesis tested was that circulating EPCs are reduced in young people with type 1 diabetes without vascular injury and that this is associated with impaired endothelial function and increased carotid intima-media thickness (CIMT). Methods We compared 74 people with type 1 diabetes with 80 healthy controls. CD34, CD133, vascular endothelial (VE) growth factor receptor-2 (VEGFR-2) and VE-cadherin antibodies were used to quantify EPCs and progenitor cell subtypes using flow-cytometry. Ultrasound assessment of endothelial function by brachial artery flow-mediated dilatation (FMD) and CIMT was made. Circulating endothelial markers, inflammatory markers and plasma plasminogen activator inhibitor-1 (PAI-1) levels were measured. Results CD34+VE-cadherin+, CD133+VE-cadherin+ and CD133+VEGFR-2+ EPC counts were significantly lower in people with diabetes (46-69%; p=0.004-0.043). In people with type 1 diabetes, FMD was reduced by 45% (p<0.001) and CIMT increased by 25% (p<0.001), these being correlated (r=−0.25, p=0.033). There was a significant relationship between FMD and CD34+VE-cadherin+ (r = 0.39, p = 0.001), CD133+VEGFR-2+ (r =0.25, p = 0.037) and CD34+ (r=0.34, p=0.003) counts. Circulating high-sensitivity C-reactive protein, PAI-1, interleukin-6 and E-selectin were significantly higher in the diabetes group (p < 0.001 to p = 0.049), the last two of these correlating with FMD (r=−0.27, p=0.028 and r=−0.24, p=0.048, respectively). Conclusions/interpretation These findings suggest that abnormalities of endothelial function in addition to proinflammatory and pro-thrombotic states are already common in people with type 1 diabetes before development of clinically evident arterial damage. Low EPC counts confirm risk of macrovascular complications and may account for impaired endothelial function and predict future cardiovascular events.

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“…Both studies showed that a symptom-limited treadmill or bicycle exercise test could acutely increase the amount of EPCs. Possible mechanisms for this fast increase in EPCs (10 min to 2 h) may be an exercise-induced increase of VEGF (8,72) or exerciseinduced changes in shear stress, resulting in mobilization of the cells (73). Since all these studies investigated the effect of a single exercise bout on the mobilization of EPCs, one has to ask the question if ET over a longer time period also can influence the number and function of EPCs.…”

Section: Physical Exercisementioning

confidence: 99%

Endothelial progenitor cells: Implications for cardiovascular disease

et al. 2008

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Exercise acutely increases circulating endothelial progenitor cells and monocyte-/macrophage-derived angiogenic cells

Abstract: Our study demonstrates that exercise can acutely increase EPCs and CACs. Given the ability of these cell populations to promote angiogenesis and vascular regeneration, the exercise-induced cell mobilization may serve as a physiologic repair or compensation mechanism.

Cited by 287 publications

References 17 publications

Flow cytometric evaluation of circulating endothelial cells: A new protocol for identifying endothelial cells at several stages of differentiation

Flow cytometric evaluation of circulating endothelial cells: A new protocol for identifying endothelial cells at several stages of differentiation

Circulating endothelial progenitor cells, endothelial function, carotid intima–media thickness and circulating markers of endothelial dysfunction in people with type 1 diabetes without macrovascular disease or microalbuminuria

Endothelial progenitor cells: Implications for cardiovascular disease

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