Estradiol, acting through ERα, induces endothelial non-classic renin-angiotensin system increasing angiotensin 1–7 production

Mompeón, Ana; Lázaro-Franco, Macarena; Bueno-Betí, Carlos; Pérez‐Cremades, Daniel; Vidal‐Gómez, Xavier; Monsalve, Elena; Gironacci, Mariela M.; Hermenegildo, Carlos; Novella, Susana

doi:10.1016/j.mce.2015.11.004

Cited by 62 publications

(55 citation statements)

References 42 publications

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“…It has been also reported that vascular smooth muscle cells proliferation is inhibited through an ERα-dependent miR-203 up-regulation [60]. Specifically, estrogen action in endothelial cells is assumed to be mainly mediated by ERα [6,7,28].…”

Section: Discussionmentioning

confidence: 99%

“…Control cells were exposed to the same vehicle of cells treated with E2 (0.1% etanol) or antagonist (0.1% DMSO). All concentrations and times selected were chosen taking into account previous studies [5,19,20]. A schematic workflow of the experimental design is provided in Fig.…”

Section: Cell Culture and Experimental Designmentioning

confidence: 99%

“…Protective effects by estrogen on cardiovascular system have been related to increased vasodilation, anti-inflammatory action, regulation of vascular smooth muscle cell proliferation, and attenuation of atherosclerotic processes [4]. In this regard, the E2-mediated vasoprotective role through an increase of endothelial-derived factors has been described to be ER-dependent [5][6][7].…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA as Crucial Regulators of Gene Expression in Estradiol-Treated Human Endothelial Cells

Vidal‐Gómez

Pérez‐Cremades

Mompeón

et al. 2018

Cell Physiol Biochem

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Background/Aims: Estrogen signalling plays an important role in vascular biology as it modulates vasoactive and metabolic pathways in endothelial cells. Growing evidence has also established microRNA (miRNA) as key regulators of endothelial function. Nonetheless, the role of estrogen regulation on miRNA profile in endothelial cells is poorly understood. In this study, we aimed to determine how estrogen modulates miRNA profile in human endothelial cells and to explore the role of the different estrogen receptors (ERα, ERβ and GPER) in the regulation of miRNA expression by estrogen. Methods: We used miRNA microarrays to determine global miRNA expression in human umbilical vein endothelial cells (HUVEC) exposed to a physiological concentration of estradiol (E2; 1 nmol/L) for 24 hours. miRNAgene interactions were computationally predicted using Ingenuity Pathway Analysis and changes in miRNA levels were validated by qRT-PCR. Role of ER in the E2-induced miRNA was additionally confirmed by using specific ER agonists and antagonists. Results: miRNA array revealed that expression of 114 miRNA were significantly modified after E2 exposition. Further biological pathway analysis revealed cell death and survival, lipid metabolism, reproductive system function, as the top functions regulated by E2. We validated changes in the most significantly increased (miR-30b-5p, miR-487a-5p, miR-4710, miR-501-3p) and decreased (miR-378h and miR-1244) miRNA and the role of ER in these E2-induced miRNA was determined. Results showed that both classical, ERα and ERβ, and membrane-bound ER, GPER, differentially regulated specific miRNA. In silico analysis of validated miRNA promoters identified specific ER binding sites. Conclusion: Our findings identify differentially expressed miRNA pathways linked to E2 in human endothelial cells through ER, and provide new insights by which estrogen can modulate endothelial function.

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Section: Discussionmentioning

confidence: 99%

Section: Cell Culture and Experimental Designmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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MicroRNA as Crucial Regulators of Gene Expression in Estradiol-Treated Human Endothelial Cells

Vidal‐Gómez

Pérez‐Cremades

Mompeón

et al. 2018

Cell Physiol Biochem

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“…The roles of estrogen in the tuning of AT levels in vitro are controversial. Various studies reported that supplementation of E 2 could induce increase [9,11] or decrease [22,23] of the expression of AT system member genes. In our results, E 2 -treated group showed lower expression of AT II than control group.…”

Section: Discussionmentioning

confidence: 99%

“…results in a decrease in AT receptors [8]. It increases AT production [9], and its increased secretion is associated with increased expression levels of AT receptor mRNA and protein [10][11][12].…”

Section: Introductionmentioning

confidence: 99%

Effects of Estradiol on the Paracrine Regulator Expression of In Vitro Maturated Murine Ovarian Follicles

Kim

Park

Kim

et al. 2017

Tissue Eng Regen Med

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The preservation of female germ cells is important in the individuals with ovarian dysfunction and failure. For this purpose, ovarian follicle in vitro maturation (OFIVM) is an important technology for the retrieval of mature oocytes. In the in vivo follicular development, paracrine factors such as angiotensin (AT) and anti-Müllerian hormone (AMH) play important roles. We attempted to add estrogen during the OFIVM and to assess their expression on the follicular cells. The ovaries and pre-antral follicles were collected from 13-day C57BL/6 mice and cultured in vitro with estradiol (E 2 ) treatment for up to two weeks. In the whole ovaries, the expression of AT II was decreased and the expression of AMH was similar between control and E 2 -treated ovaries after in vitro culture. Although there was no difference in the survival, ovulation, maturation and fertilization rates between control and E 2 -treated groups, the expression of AT II in the follicular cells was down-regulated after E 2 treatment at mRNA level, and AMH showed similar expression. In conclusion, adding E 2 in OFIVM may regulate paracrine factors and their receptors that are related to follicular development. Further investigations are necessary to elucidate the roles of various sex hormones in the regulation of AT and AMH expression during the OFIVM.

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The Angiotensin-(1-7) Axis: Formation and Metabolism Pathways

Chappell

2019

Angiotensin-(1-7)

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Estradiol, acting through ERα, induces endothelial non-classic renin-angiotensin system increasing angiotensin 1–7 production

Cited by 62 publications

References 42 publications

MicroRNA as Crucial Regulators of Gene Expression in Estradiol-Treated Human Endothelial Cells

MicroRNA as Crucial Regulators of Gene Expression in Estradiol-Treated Human Endothelial Cells

Effects of Estradiol on the Paracrine Regulator Expression of In Vitro Maturated Murine Ovarian Follicles

The Angiotensin-(1-7) Axis: Formation and Metabolism Pathways

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