Human CD34+AC133+VEGFR-2+ cells are not endothelial progenitor cells but distinct, primitive hematopoietic progenitors

Case, Jamie; Mead, Laura E.; Bessler, Waylan; Prater, Daniel N.; White, Hilary; Saadatzadeh, M. Reza; Bhavsar, Janak R.; Yoder, Mervin C.; Haneline, Laura S.; Ingram, David A.

doi:10.1016/j.exphem.2007.04.002

Cited by 500 publications

(426 citation statements)

References 44 publications

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“…The combined expression of CD133 and VEGFR2 is widely thought to characterize early functional EPCs, 7,8 although this notion has recently been questioned. 9 While VEGFR2 is expressed on both mature ECs and their progenitors, CD133 distinguishes EPCs from mature ECs sloughed from injured vessel walls. CD133 expression also sets EPCs apart from CD34 À / CD14 + cells of myelomonocytic lineage that can 'transdifferentiate' into endothelial-like cells, which appear to be effective for re-endotheliazation when given intravenously (i.v.)…”

mentioning

confidence: 99%

Endothelial progenitor cells for cancer gene therapy

2008

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confidence: 99%

Endothelial progenitor cells for cancer gene therapy

2008

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“…ECFC, also called late outgrowth EPC, can form well‐defined cobblestone‐patterned colonies from days 7 to 30 in culture 13, 19. Unlike hematopoietic progenitor cells, ECFC do not express CD133 and CD45 19, 35. However, the presence of CD34 and CD31 markers added to their clonogenic and vasculogenic potential confers to these cells a progenitor and endothelial phenotype 19.…”

Section: Discussionmentioning

confidence: 99%

Endothelial Colony‐Forming Cells in Young Adults Born Preterm: A Novel Link Between Neonatal Complications and Adult Risks for Cardiovascular Disease

Bertagnolli

Xie

Paquette

et al. 2018

JAHA

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BackgroundPreterm birth is linked to cardiovascular risks and diseases. Endothelial progenitor cells play a critical role in vascular development and repair. Cord blood endothelial progenitor cells of preterm‐born infants, especially endothelial colony‐forming cells (ECFC), show enhanced susceptibility to prematurity‐related pro‐oxidant stress. Whether ECFC dysfunction is present in adulthood following preterm birth is unknown.Methods and ResultsThis cross‐sectional observational study includes 55 preterm‐born (≤29 gestational weeks) young adults (18–29 years old, 38% male) and 55 sex‐ and age‐matched full‐term controls. ECFC were isolated from peripheral blood; cell proliferative and vascular cord formation capacities were assessed in vitro. Daytime systolic blood pressure was higher, whereas glucose tolerance and body mass index were lower in preterm‐born subjects. ECFC colonies grew in culture for 62% of full‐term‐ and 58% of preterm‐born participants. Preterm‐born participants have formed ECFC colonies later in culture and have reduced proliferation compared with controls. Only in preterm‐born individuals, we observed that the later the ECFC colony grows in culture, the worse was overall ECFC function. In addition, in preterms, elevated systolic blood pressure significantly correlated with reduced ECFC proliferation (rS=−0.463; P=0.030) and numbers of branches formed on matrigel (rS=−0.443; P=0.039). In preterm‐born subjects, bronchopulmonary dysplasia was associated with impaired ECFC function, whereas exposure to antenatal steroids related to better ECFC function.ConclusionsThis study is the first to examine ECFC in preterm‐born adults and to demonstrate ECFC dysfunction compared with full‐term controls. In the preterm‐born group, ECFC dysfunction was associated with bronchopulmonary dysplasia, the major prematurity‐related neonatal morbidity, and with increased systolic blood pressure into adulthood.

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“…However, few studies have attempted to formally compare the functional properties of this EPC subset in hematopoietic and endothelial clonogenic assays to gain more insight in the biology of the phenotype used, namely to assess the identity of their clonal progeny, which participates in vessel repair. 17,18 No clear evidence has been reported about the existence of specific markers, which allows to prospectively isolate EPCs with a phenotype superior to the one so far described. 18 In patients with ED, the number of EPCs with the phenotype CD34 pos /CD133 pos /KDR pos is reduced and this reduction seems to be greater in presence of cardiovascular risk factors (cigarette smoke, hypertension, diabetes mellitus, obesity and dyslipidemia).…”

Section: Discussionmentioning

confidence: 99%

“…21 It is now clear that there are distinct EPC sub-populations with different phenotype and biological properties. 6 Cells progress from stem cell stage to the final mature cell of each single lineage, through successive progenitor cell stages, 23 and because uniform criteria to identify these cells are lacking, we followed the proposal outlined by Case et al 17 They suggested to use the CD45 neg / CD34 pos phenotype, because these cells form colonies of mature endothelial cells in a clonogenic in-vitro assay of endothelial cells. Therefore, probably these cells behave to a greater extent as true endothelial progenitors 19 and accordingly, CD45 neg /CD34 pos / CD144 pos cells form endothelial cells in culture.…”

Section: Discussionmentioning

confidence: 99%

Original evaluation of endothelial dysfunction in men with erectile dysfunction and metabolic syndrome

et al. 2012

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We have recently demonstrated the diagnostic value of a new immunophenotype of blood endothelial progenitor cells (EPCs ¼ CD45neg/CD34pos/CD144pos) and endothelial microparticles (EMPs ¼ CD45neg/CD144pos/AnnexinVpos) in patients with arterial erectile dysfunction (ED) according to severity of cavernous arterial insufficiency evaluated through penile Doppler. The aim of this study was to evaluate both EPCs and EMPs in patients with arterial ED and metabolic syndrome (MetS), comparing these patients with another group of patients without MetS and ED and a third group with MetS but without ED. For this study 50 patients with arterial ED and MetS were selected (age: 55.0±3.0 years; range: 47--60). A group of age-matched (age: 54.0 ± 2.0 years; range: 44--60) patients without arterial ED and MetS INTRODUCTIONWe have recently demonstrated the diagnostic value of a new immunophenotype of blood endothelial progenitor cells (EPCs ¼ CD45neg/CD34pos/CD144pos) and endothelial microparticles (EMPs ¼ CD45neg/CD144pos/AnnexinVpos) in patients with arterial erectile dysfunction (ED) according to severity of cavernous arterial insufficiency evaluated through penile Doppler, showing that serum concentrations of these immunophenotypes are significantly higher compared with patients with psychogenic ED and among patients with arterial ED, those with severe arterial insufficiency showed significantly higher serum concentrations of EPCs and EMPs. 1 On this basis, the present study was undertaken to evaluate the number of EPCs and EMPs in patients with metabolic syndrome (MetS) and ED of arterial origin, which is a very common category among patients with sexual dysfunction in clinical practice. This clinical model seemed to us suitable to gain more insight into the balance between bone marrow endothelial repair mechanism and endothelial dysfunction in the manifestation of the clinical symptoms. To accomplish this, 50 patients with arterial dysfunctional-based ED and MetS, established by the Adult Treatment Panel (ATP) III criteria (NCEP ATPIII, 2002), were selected and the number of circulating EPCs and EMPs was determined. Two different groups of patients were enrolled as control: (a) patients without arterial ED and MetS; and (b) patients with MetS but without ED.

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Human CD34+AC133+VEGFR-2+ cells are not endothelial progenitor cells but distinct, primitive hematopoietic progenitors

Cited by 500 publications

References 44 publications

Endothelial progenitor cells for cancer gene therapy

Endothelial progenitor cells for cancer gene therapy

Endothelial Colony‐Forming Cells in Young Adults Born Preterm: A Novel Link Between Neonatal Complications and Adult Risks for Cardiovascular Disease

Original evaluation of endothelial dysfunction in men with erectile dysfunction and metabolic syndrome

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