Estradiol Stimulates Capillary Formation by Human Endothelial Progenitor Cells

Baruscotti, Isabella; Barchiesi, Federica; Jackson, Edwin K.; Imthurn, Bruno; Stiller, Ruth; Kim, Jai-Hyun; Schaufelberger, Sara; Rosselli, Marinella; Hughes, Christopher C.W.; Dubey, Raghvendra K.

doi:10.1161/hypertensionaha.110.153262

Cited by 38 publications

(18 citation statements)

References 24 publications

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“…39 Estrogen also improves endothelial and myocardial function after ischemia by an antiapoptotic and pro-survival effect on cardiomyocytes, 40,41 endothelial progenitor cell mobilization 42 and mesenchymal stem cell-mediated vascular endothelial growth factor release. 43,44 These rapid effects of estrogen on the action of CF6 were not examined in this study. However, CF6 attenuates prostacyclin generation via the inhibition of cytosolic phospholipase A 2 , 16 nitric oxide generation via the upregulation of asymmetric dimethylarginine or the inhibition of endothelial nitric oxide synthase phosphorylation 45,46 and the PI3K/Akt cascade.…”

Section: Discussionmentioning

confidence: 99%

Estrogen attenuates coupling factor 6-induced salt-sensitive hypertension and cardiac systolic dysfunction in mice

et al. 2012

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In male coupling factor 6 (CF6)-overexpressing transgenic (TG) mice, a high-salt diet induces hypertension and cardiac systolic dysfunction with excessive reactive oxygen species generation. However, the role of gender in CF6-mediated pathophysiology is unknown. We investigated the effects of ovariectomy and estrogen replacement on hypertension, cardiac dysfunction and Rac1 activity, which activates radical generation and the mineralocorticoid receptor, in female TG mice. Fifteen-week-old male and female TG and wild-type (WT) mice were fed a normal-or high-salt diet for 60 weeks. Systolic and diastolic blood pressures were higher in the TG mice fed a high-salt diet than in those fed a normal-salt diet at 20-60 weeks in males but only at 60 weeks in females. The blood pressure elevation under high-salt diet conditions was concomitant with a decrease in left ventricular fractional shortening. In the WT mice, neither blood pressure nor cardiac systolic function was influenced by a high-salt diet. In the female TG mice, bilateral ovariectomy induced hypertension with cardiac systolic dysfunction 8 weeks after the initiation of a high-salt diet. The ratios of Rac1 bound to guanosine triphosphate (Rac1-GTP) to total Rac1 in the heart and kidneys were increased in the ovariectomized TG mice, and estrogen replacement abolished the CF6-mediated pathophysiology induced under the high-salt diet conditions. The overexpression of CF6 induced salt-sensitive hypertension, complicated by systolic cardiac dysfunction, but its onset was delayed in females. Estrogen has an important role in the regulation of CF6-mediated pathophysiology, presumably via the downregulation of Rac1. Hypertension Research (2012) 35, 539-546; doi:10.1038/hr.2011.232; published online 19 January 2012Keywords: coupling factor 6; estrogen; heart failure; hypertension; salt INTRODUCTION Premenopausal women have a lower risk and incidence of hypertension and cardiovascular disease than age-matched men. However, this gender advantage gradually disappears after menopause. Although blood pressure is lower in premenopausal women than in men, after menopause, it increases to levels similar to or higher than those of agematched men. 1,2 The recent Nurse's Health Study 3 and WISE Study, 4 as well as others, 5 have demonstrated that compared with women with normal endogenous estrogen levels, young women undergoing early menopause owing to ovarian dysfunction or bilateral ovariectomy have an increased risk of cardiovascular disease. In animal models of cardiovascular disease, females exhibited lower mortality, less vascular injury, better preservation of cardiovascular function, and slower progression to decompensated heart failure than did males, although such differences were abolished after ovariectomy or induction of a deficiency in endogenous estrogen. 6,7-9 These findings clearly suggest that sex hormones have a cardioprotective role in women. Although randomized, prospective, primary or secondary prevention trials failed

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Section: Discussionmentioning

confidence: 99%

Estrogen attenuates coupling factor 6-induced salt-sensitive hypertension and cardiac systolic dysfunction in mice

et al. 2012

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“…Their differentiation capacity is being questioned and more data indicate for rather paracrine effect of those cells, named currently proangiogenic cells (239). Nevertheless, it has been convincingly demonstrated that HO-1 improved re-endothelialization both after pharmacological (16,232) or genetic (129) induction, the process in which EPCs could play a role. HO-1 induction by probucol and succinobucol increased both the bone-marrowlocated and the released EPCs (232), which formed also more colonies, while differentiation of EPCs from knockout mice was impaired (232).…”

Section: Endothelial Progenitor Cellsmentioning

confidence: 99%

Role of Heme Oxygenase-1 in Postnatal Differentiation of Stem Cells: A Possible Cross-Talk with MicroRNAs

Kozakowska

Szade

Dulak

et al. 2014

Antioxidants & Redox Signaling

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Significance: Heme oxygenase-1 (HO-1) converts heme to biliverdin, carbon monoxide, and ferrous ions, but its cellular functions are far beyond heme metabolism. HO-1 via heme removal and degradation products acts as a cytoprotective, anti-inflammatory, immunomodulatory, and proangiogenic protein, regulating also a cell cycle. Additionally, HO-1 can translocate to nucleus and regulate transcription factors, so it can also act independently of enzymatic function. Recent Advances: Recently, a body of evidence has emerged indicating a role for HO-1 in postnatal differentiation of stem and progenitor cells. Maturation of satellite cells, skeletal myoblasts, adipocytes, and osteoclasts is inhibited by HO-1, whereas neurogenic differentiation and formation of cardiomyocytes perhaps can be enhanced. Moreover, HO-1 influences a lineage commitment in pluripotent stem cells and maturation of hematopoietic cells. It may play a role in development of osteoblasts, but descriptions of its exact effects are inconsistent. Critical Issues: In this review we discuss a role of HO-1 in cell differentiation, and possible HO-1-dependent signal transduction pathways. Among the potential mediators, we focused on microRNA (miRNA). These small, noncoding RNAs are critical for cell differentiation. Recently we have found that HO-1 not only influences expression of specific miRNAs but also regulates miRNA processing enzymes. Future Directions: It seems that interplay between HO-1 and miRNAs may be important in regulating fates of stem and progenitor cells and needs further intensive studies.

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“…1). Moreover, estrogen has been shown to promote endothelial progenitor cell mobilization [44] and enhance mesenchymal stem cell-mediated vascular endothelial growth factor (VEGF) release [45,46 • ], improving endothelial and myocardial functional after ischemia.…”

Section: Cardioprotective Mechanisms Of Estrogenmentioning

confidence: 99%

Estrogen, hormonal replacement therapy and cardiovascular disease

Yang

Reckelhoff

2011

Current Opinion in Nephrology &Amp; Hypertension

224

150

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Purpose of review Premenopausal women have a lower risk and incidence of hypertension and cardiovascular disease (CVD) compared to age-matched men and this sex advantage for women gradually disappears after menopause, suggesting that sexual hormones play a cardioprotective role in women. However, randomized prospective primary or secondary prevention trials failed to confirm that hormone replacement therapy (HRT) affords cardioprotection. This review highlights the factors that may contribute to this divergent outcome and could reveal why young or premenopausal women are protected from CVD and yet postmenopausal women do not benefit from HRT. Recent findings In addition to the two classical estrogen receptors, ERα and ERβ, a third, G-protein-coupled estrogen receptor GPR30, has been identified. New intracellular signaling pathways and actions for the cardiovascular protective properties of estrogen have been proposed. In addition, recent Women’s Health Initiative (WHI) studies restricted to younger postmenopausal women showed that initiation of HRT closer to menopause reduced the risk of CVD. Moreover, dosage, duration, the type of estrogen and route of administration all merit consideration when determining the outcome of HRT. Summary HRT has become one of the most controversial topics related to women’s health. Future studies are necessary if we are to understand the divergent published findings regarding HRT and develop new therapeutic strategies to improve the quality of life for women.

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Estradiol Stimulates Capillary Formation by Human Endothelial Progenitor Cells

Cited by 38 publications

References 24 publications

Estrogen attenuates coupling factor 6-induced salt-sensitive hypertension and cardiac systolic dysfunction in mice

Estrogen attenuates coupling factor 6-induced salt-sensitive hypertension and cardiac systolic dysfunction in mice

Role of Heme Oxygenase-1 in Postnatal Differentiation of Stem Cells: A Possible Cross-Talk with MicroRNAs

Estrogen, hormonal replacement therapy and cardiovascular disease

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