Influence of menstrual cycle on circulating endothelial progenitor cells

Robb, Amy O.; Mills, Nicholas L; Smith, Imogen; Short, Abigail; Tura-Ceide, Olga; Barclay, G. R.; Blomberg, Anders; Critchley, Hilary O. D.; Newby, David E.; Denison, Fiona C.

doi:10.1093/humrep/den411

Cited by 45 publications

(32 citation statements)

References 33 publications

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“…As previously described [9,20,21], 5 · 10 6 unmodified MNCs were resuspended in EndoCult Liquid Medium (Stem Cell Technologies) and plated on fibronectin-coated six-well plates (Becton Dickinson) for 2 days. The non-adherent cells were recovered, resuspended in fresh medium, and transferred to a fibronectin-coated 24-well plate (Becton Dickinson) at 1 · 10 6 per well in the presence or absence of G-CSF (100 ng mL ) for a further 3 days; the colonies per well were then counted, and the EPC frequency was calculated.…”

Section: Cfu-epcsmentioning

confidence: 99%

“…True EPCs are defined as cells that, in culture over 3-4 weeks on collagen, can give rise to endothelial outgrowth cells (EOCs) [14][15][16], whereas cells that give rise over 5-6 days to colonies on fibronectin (colony-forming unit endothelial progenitor cells) (CFU-EPCs), formerly proposed to be EPCs [17], are now recognized to be generated by monocytes [16,18,19]. CFUEPCs stain for many endothelial markers [20,21] but also retain CD14 expression [22]. Monocytes can themselves mimic endothelial cells (ECs) by upregulating expression of many markers held to be endothelial, and have probably been mistaken for ECs in many investigations [22,23].…”

Section: Introductionmentioning

confidence: 99%

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Granulocyte colony‐stimulating factor (G‐CSF) depresses angiogenesis in vivo and in vitro: implications for sourcing cells for vascular regeneration therapy

Tura

Crawford

Barclay

et al. 2010

Journal of Thrombosis and Haemostasis

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Summary. Background: The most common source of hematopoietic progenitor cells (HPCs) for hematopoietic reconstitution comprises granulocyte colony‐stimulating factor (G‐CSF)‐mobilized peripheral blood stem cells (PBSCs). It has been proposed that endothelial progenitor cells (EPCs) share precursors with HPCs, and that EPC release may accompany HPC mobilization to the circulation following G‐CSF administration. Objective: To investigate EPC activity following HPC mobilization, and the direct effects of exogenous G‐CSF administration on human umbilical vein endothelial cells (HUVECs) and endothelial outgrowth cells (EOCs), using in vitro and in vivo correlates of angiogenesis. Patients/Methods: Heparinized venous blood samples were collected from healthy volunteers and from cord blood at parturition. G‐CSF‐mobilized samples were collected before administration, at apheresis harvest, and at follow‐up. PBSCs were phenotyped by flow cytometry, and cultured in standard colony‐forming unit (CFU)‐EPC and EOC assays. The effect of exogenous G‐CSF was investigated by addition of it to HUVECs and EOCs in standard tubule formation and aortic ring assays, and in an in vivo sponge implantation model. Results: Our data show that G‐CSF mobilization of PBSCs produces a profound, reversible depression of circulating CFU‐EPCs. Furthermore, G‐CSF administration did not mobilize CD34+CD133− cells, which include precursors of EOCs. No EOCs were cultured from any mobilized PBSCs studied. Exogenous G‐CSF inhibited CFU‐EPC generation, HUVEC and EOC tubule formation, microvessel outgrowth, and implanted sponge vascularization in mice. Conclusions: G‐CSF administration depresses both endothelial cell angiogenesis and monocyte proangiogenic activity, and we suggest that any angiogenic benefit observed following implantation of cells mobilized by G‐CSF may come only from a paracrine effect from HPCs.

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Section: Cfu-epcsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Granulocyte colony‐stimulating factor (G‐CSF) depresses angiogenesis in vivo and in vitro: implications for sourcing cells for vascular regeneration therapy

Tura

Crawford

Barclay

et al. 2010

Journal of Thrombosis and Haemostasis

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“…In rodents, E 2 increases the number of circulating EPCs and enhances their adherence and homing to the region of vascular damage. Likewise, in premenopausal women the number of circulating EPCs is synchronized with the menstrual cycle and is highest during the fertile period [Robb et al 2009;Foresta et al 2008]. Furthermore, EPCs in men reportedly showed a lower adherence capacity than those in premenopausal women, an effect that was abolished by E 2 supplementation [Fadini et al 2008].…”

Section: Senescent Bone Marrow-derived Epcs and Impairment Of Cardiovmentioning

confidence: 99%

Endothelial progenitor cell senescence is there a role for estrogen?

Imanishi

Tsujioka

2009

Therapeutic Advances in Cardiovascular Disease

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Recent studies have demonstrated that aging or senescence constitutes a potential limitation to the ability of endothelial progenitor cells (EPCs) to sustain ischemic tissue repair. Excess amount of reactive oxygen species (ROS) is involved in senescence, causing defective neovascularization. Conversely, estrogens have been shown to accelerate recovery of the endothelium after vascular injury. Estrogen reduces EPC senescence through augmentation of telomerase activity. In addition, the inhibition of EPC senescence by estrogen in vitro may improve the functional activity of EPCs in a way that is important for potential cell therapy. This review describes current understanding of EPC senescence and the role of estrogen in preventing EPC senescence.Keywords: endothelial progenitor cell, estrogen, senescence, telomerase IntroductionThe lower incidence of cardiovascular disease (CVD) in premenopausal women than in men may be attributable, at least in part, to estrogen [Dubey and Jackson, 2001;Mendelsohn and Karas, 1999;Nathan and Chaudhuri, 1997; Farhat et al. 1996]. Premenopausal women are at a lower risk for atherosclerosis and thus have a lower incidence of coronary heart disease and myocardial infarction than postmenopausal women or age-matched men. It has long been postulated that the concentration of circulating 17b-estradiol (E 2 ) plays an important role in the gender-specific cardioprotective effect; however, the underlying mechanism of action of E 2 remains a matter of debate. Relevant biological effects of estrogens are numerous and include, for example, an improvement in lipid and lipoprotein profiles and endothelium-dependent vasodilation triggered by E 2 at physiological concentration.

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“…Studies have demonstrated that EPC levels vary with age, gender, smoking and certain conditions such as diabetes, hypertension and/or other cardiovascular diseases. Robb et al demonstrated that EPC levels even vary during the menstrual cycle in a potential effort to repair the uterine endometrium 33 . Thus, studies involving measurement of EPC are affected by high individual variability, and study design should aim to reduce this by taking into account the variables described below.…”

Section: Why Do Epc Numbers Differ Among Studies Involving Copd Patiementioning

confidence: 99%

Endothelial progenitor cells in chronic obstructive pulmonary disease

Tura-Ceide¹

2013

OA Stem Cells

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Influence of menstrual cycle on circulating endothelial progenitor cells

Cited by 45 publications

References 33 publications

Granulocyte colony‐stimulating factor (G‐CSF) depresses angiogenesis in vivo and in vitro: implications for sourcing cells for vascular regeneration therapy

Granulocyte colony‐stimulating factor (G‐CSF) depresses angiogenesis in vivo and in vitro: implications for sourcing cells for vascular regeneration therapy

Endothelial progenitor cell senescence is there a role for estrogen?

Endothelial progenitor cells in chronic obstructive pulmonary disease

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