Role of estrogen receptors in menstrual cycle–related neoangiogenesis and their influence on endothelial progenitor cell physiology

Toni, Luca De; Mambro, Antonella Di; Ferlin, Alberto; Perilli, Lisa; Bertuzzi, Ilaria; Galan, Alessandro; Zuccarello, Daniela

doi:10.1016/j.fertnstert.2008.09.059

Cited by 21 publications

(13 citation statements)

References 38 publications

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“…This inconsistency could be due to the different protocols of EPCs isolation that, as mentioned above, could lead to very different experimental results. Moreover Recently, it has been showed that estrogens have indeed a physiological role in modulating the biology and kinetics of EPCs: cyclic EPCs mobilization mirrored estrogens kinetics during the menstrual cycle in fertile females and EPCs were incorporated into vasculature of the endometrium [144][145][146]. Moreover, estrogens potently regulate EPCs bioactivity in terms of enhanced proliferation, migration, differentiation and reduced apoptosis; these effects were abolished treating EPCs with the pharmacologic estrogen receptor inhibitor ICI, proving that estrogens clearly regulate EPCs [146].…”

Section: Epcs and Sex Hormonesmentioning

confidence: 97%

Pharmacologic Targeting of Endothelial Progenitor Cells

Albiero¹,

Menegazzo²,

Avogaro³

et al. 2010

CHDDT

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The endothelium entered the field of regenerative medicine with the discovery of endothelial progenitor cells (EPCs). These cells participate in endothelial homeostasis and are actively involved in physiological and pathological neovascularization. Despite the unresolved discussion about the very phenotype of these cells, great efforts have been devoted to study the role of EPCs in cardiovascular diseases. EPCs are very rare in peripheral circulation and are further reduced in association with cardiovascular diseases. Therefore, finding therapies to improve EPCs could unleash the way to promising cell-based therapies. Ex-vivo expansion of EPCs is a critical step to augment EPCs number, but it still needs several improvements. An alternative strategy to partially overcome these limitations is to target EPCs with available drugs. In this review we will discuss how disparate pharmacological compounds have been used to improve EPCs number and functions.

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Section: Epcs and Sex Hormonesmentioning

confidence: 97%

Pharmacologic Targeting of Endothelial Progenitor Cells

Albiero¹,

Menegazzo²,

Avogaro³

et al. 2010

CHDDT

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“…Exclusion criteria comprised AMI within the previous 2 weeks or the use of a DES. Women were similarly excluded to avoid estrogen-dependent effects such as increased EPC numbers, leading to accelerated reen- dothelialization and diminished neointima formation after arterial injury [174,175] and to avoid potential confounding effects by menstrual cycle or postmenopausa [176][177][178]. Peripheral blood samples for CD34 + evaluation were drawn at baseline (before stenting) and 1 day after stenting.…”

Section: Restenosismentioning

confidence: 99%

Role of Endothelial Progenitor Cell Mobilization After Percutaneous Angioplasty Procedure

Barsotti

Stefano²,

Spontoni³

et al. 2009

CPD

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Circulating endothelial progenitor cells (EPCs) are bone marrow-derived cells, contributing to endothelial cell regeneration of injured vessels as well as neovascularization of ischemic lesions. EPC levels and function are inversely correlated with cardiovascular risk factors, can predict the occurrence of adverse events and atherosclerotic disease progression. Ischemia and inflammation are the primary triggers for EPC mobilization and homing, however, vascular trauma, as it occurs during surgical procedures, has been demonstrated to stimulate EPC mobilization even in absence of tissue ischemia. The effect of angioplasty on EPCs is not well defined, mainly because of the different and sometimes contrasting clinical results, due to low numbers of patients enrolled and to lack of standardization in evaluating EPCs. Aim of this review is to report recent results on the effect of EPC mobilization and homing after angioplasty, attempting to summarize them in a comprehensive model. The effect on EPCs of different kind of stents and the potential use of new stents able to attract EPCs will be also described. Results obtained in patients undergoing angioplasty in different vascular districts (coronary, peripheral and carotid) will be shown, together with the correlation between circulating progenitor cells and restenosis.

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“…Recently it has been demonstrated that estrogen receptor (ER) is expressed in EPCs in vivo and in vitro (Baruscotti et al, 2010). EPCs proliferation is induced during the menstrual phase and the proliferation can be affected by estrogen through ERα activation (Foresta et al, 2010). These studies suggested the potential regulation of stem cells by sex steroids.…”

Section: Introductionmentioning

confidence: 99%

Chemoattraction of bone marrow-derived stem cells towards human endometrial stromal cells is mediated by estradiol regulated CXCL12 and CXCR4 expression

et al. 2015

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Bone marrow derived cells engraft to the uterine endometrium and contribute to endometriosis. The mechanism by which these cells are mobilized and directed to the endometrium has not been previously characterized. We demonstrate that human endometrial stromal cells (hESCs) produce the chemokine CXCL12 and that bone marrow cells (BMCs) express the CXCL12 receptor, CXCR4. Treatment with physiological levels of estradiol (E2) induced both CXCL12 and CXCR4 expression in hESCs and BMCs, respectively. BMCs migrated towards hESCs conditioned media; a CXCR4 antagonist blocked migration indicating that CXCL12 acting through its receptor, CXCR4, is necessary for chemoattraction of BM cells to human endometrial cells. E2 increased both CXCL12 expression in endometrial cells and CXCR4 expression in BM cells, further enhancing chemoattraction. E2 induced CXCL12/CXCR4 expression in endometrium and BM, respectively, drives migration of stem cells to the endometrium. The E2-CXCL12/CXCR4 signaling pathway may be useful in determining treatments for endometrial disorders, and may be antagonized to block stem cell migration to endometriosis.

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Role of estrogen receptors in menstrual cycle–related neoangiogenesis and their influence on endothelial progenitor cell physiology

Cited by 21 publications

References 38 publications

Pharmacologic Targeting of Endothelial Progenitor Cells

Pharmacologic Targeting of Endothelial Progenitor Cells

Role of Endothelial Progenitor Cell Mobilization After Percutaneous Angioplasty Procedure

Chemoattraction of bone marrow-derived stem cells towards human endometrial stromal cells is mediated by estradiol regulated CXCL12 and CXCR4 expression

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