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The Role of Estrogen Receptors in Health and Disease 2.0
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The Role of Estrogen Receptors in Health and Disease 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: closed (30 June 2022) | Viewed by 11809

Special Issue Editor

Dr. Farzad Pakdel

E-Mail Website
Guest Editor
Research Institute in Health, Environment and Occupation (Irset), Inserm U1085, Transcription, Environment and Cancer Group, University of Rennes 1, 35000 Rennes, France
Interests: estrogen receptor; gene expression; transcription mechanisms; endocrine disrupter chemicals; breast cancer
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Estrogens and estrogen receptors (ERs) control a diversity of biological and physiological processes, including the growth, development, and metabolism of reproductive and non-reproductive tissues. They are also tightly associated with several human pathologies, such as breast and ovarian cancers, osteoporosis, and coronary or neurodegenerative diseases. Over the past three decades following the discovery of the nuclear ER-alpha, ER-beta, and the membrane receptor designated as the G protein-coupled estrogen receptor (GPER), multiple mechanisms of action have been identified. These mechanisms implicate either genomic actions through direct binding to specific DNA sequences, or non-genomic actions by modulating intracellular kinases cascades. The comprehension of the mechanisms underlining ER-mediated effects in the physiopathological processes is the main goal of this Special Issue. Notably, how do ERs control transcription and epigenetic regulations, and interact with intracellular kinases, coregulators of transcription, growth factors, and cellular signaling pathways to regulate cell fate, such as proliferation, differentiation, and apoptosis? What is the role of ligands, including environmental estrogens, in modulating the genomic and non-genomic activity of ERs? What are the consequence of ER mutations or the dysregulation of ER-target genes’ profiling in cancer?

In order to provide a comprehensive overview of the molecular mechanisms of ERs, researchers are invited to submit original research, comprehensive reviews, and short communications for this Special Issue, which will cover a selection of topics, highlighting the key roles of ERs in physiopatholohy.

Dr. Farzad Pakdel
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Estrogens and estrogen receptors
  • Cancer
  • Cell signaling
  • Selective estrogen receptor modulators
  • Ligand and cofactor interactions
  • Transcription and epigenetics regulation
  • Endocrine disrupter chemicals

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Related Special Issues

Published Papers (4 papers)

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Research

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13 pages, 2114 KiB  
Article
GPER Agonist G1 Prevents Wnt-Induced JUN Upregulation in HT29 Colorectal Cancer Cells
by Maria Abancens, Brian J. Harvey and Jean McBryan
Int. J. Mol. Sci. 2022, 23(20), 12581; https://doi.org/10.3390/ijms232012581 - 20 Oct 2022
Cited by 7 | Viewed by 2178
Abstract
Women consistently show lower incidence and mortality rates for colorectal cancer (CRC) compared to men. Epidemiological evidence supports a pivotal role for estrogen in protecting women against CRC. Estrogen protective effects in CRC have been mainly attributed to the estrogen receptor beta (ERβ) [...] Read more.
Women consistently show lower incidence and mortality rates for colorectal cancer (CRC) compared to men. Epidemiological evidence supports a pivotal role for estrogen in protecting women against CRC. Estrogen protective effects in CRC have been mainly attributed to the estrogen receptor beta (ERβ) however its expression is lost during CRC progression. The role of the G-protein coupled membrane estrogen receptor (GPER/GPER1/GPR30), which remains expressed after ERβ loss in CRC, is currently under debate. We hypothesise that estrogen can protect against CRC progression via GPER by modulating the Wnt/β-catenin proliferative pathway which is commonly hyperactivated in CRC. We sought evidence of sexual dimorphism within the Wnt/β-catenin pathway by conducting Kaplan–Meier analyses based on gene expression of the Wnt receptor FZD1 (Frizzled 1) in multiple public domain CRC patient data sets. High expression of FZD1 was associated with poor relapse-free survival rates in the male but not the female population. In female-derived HT29 CRC cell lines, we show that β-catenin nuclear translocation was not affected by treatment with the GPER agonist G1. However, G1 prevented the Wnt pathway-induced upregulation of the JUN oncogene. These novel findings indicate a mechanistic role for GPER in protecting against CRC progression by selectively reducing the tumorigenic effects of hyperactive Wnt/β-catenin signalling pathways in CRC. Full article
(This article belongs to the Special Issue The Role of Estrogen Receptors in Health and Disease 2.0)
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19 pages, 2915 KiB  
Article
Does G Protein-Coupled Estrogen Receptor 1 Contribute to Cisplatin-Induced Acute Kidney Injury in Male Mice?
by Eman Y. Gohar, Rawan N. Almutlaq, Chunlan Fan, Rohan S. Balkawade, Maryam K. Butt and Lisa M. Curtis
Int. J. Mol. Sci. 2022, 23(15), 8284; https://doi.org/10.3390/ijms23158284 - 27 Jul 2022
Cited by 1 | Viewed by 2273
Abstract
Nephrotoxicity is the dose-limiting side-effect of the chemotherapeutic agent cisplatin (Cp). Recent evidence points to renal protective actions of G protein-coupled estrogen receptor 1 (GPER1). In addition, it has been shown that GPER1 signaling elicits protective actions against acute ischemic injuries that involve [...] Read more.
Nephrotoxicity is the dose-limiting side-effect of the chemotherapeutic agent cisplatin (Cp). Recent evidence points to renal protective actions of G protein-coupled estrogen receptor 1 (GPER1). In addition, it has been shown that GPER1 signaling elicits protective actions against acute ischemic injuries that involve multiple organ systems; however, the involvement of GPER1 signaling in Cp-induced acute kidney injury (AKI) remains unclear. This study tested whether genetic deletion of GPER1 exacerbates Cp-induced AKI in male mice. We subjected male mice, homozygous (homo) and heterozygous (het) knockout for the GPER1 gene, and wild-type (WT) littermates to Cp or saline injections and assessed markers for renal injury on the third day after injections. We also determined serum levels of proinflammatory markers in saline and Cp-treated mice. Given the protective role of heme oxygenase-1 (HO-1) in Cp-mediated apoptosis, we also investigated genotypic differences in renal HO-1 abundance, cell death, and proliferation by Western blotting, the TUNEL assay, and Ki67 immunostaining, respectively. Cp increased serum creatinine, urea, and neutrophil gelatinase-associated lipocalin (NGAL) levels, the renal abundance of kidney injury molecule-1, and NGAL in all groups. Cp-induced AKI resulted in comparable histological evidence of injury in all genotypes. WT and homo mice showed greater renal HO-1 abundance in response to Cp. Renal HO-1 abundance was lower in Cp-treated homo, compared to Cp-treated WT mice. Of note, GPER1 deletion elicited a remarkable increase in renal apoptosis; however, no genotypic differences in cell proliferation were observed. Cp augmented kidney Ki67-positive counts, regardless of the genotype. Overall, our data do not support a role for GPER1 in mediating Cp-induced renal injury. GPER1 deletion promotes renal apoptosis and diminishes HO-1 induction in response to Cp, suggesting that GPER1 may play cytoprotective and anti-apoptotic actions in AKI. GPER1-induced regulation of HO-1 and apoptosis may offer novel therapeutic targets for the treatment of AKI. Full article
(This article belongs to the Special Issue The Role of Estrogen Receptors in Health and Disease 2.0)
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16 pages, 2459 KiB  
Article
Polyamine Oxidase Expression Is Downregulated by 17β-Estradiol via Estrogen Receptor 2 in Human MCF-7 Breast Cancer Cells
by Jin Hyung Kim and Seung-Taek Lee
Int. J. Mol. Sci. 2022, 23(14), 7521; https://doi.org/10.3390/ijms23147521 - 7 Jul 2022
Cited by 7 | Viewed by 2152
Abstract
Polyamine levels decrease with menopause; however, little is known about the mechanisms regulated by menopause. In this study, we found that among the genes involved in the polyamine pathway, polyamine oxidase (PAOX) mRNA levels were the most significantly reduced by treatment [...] Read more.
Polyamine levels decrease with menopause; however, little is known about the mechanisms regulated by menopause. In this study, we found that among the genes involved in the polyamine pathway, polyamine oxidase (PAOX) mRNA levels were the most significantly reduced by treatment with 17β-estradiol in estrogen receptor (ESR)-positive MCF-7 breast cancer cells. Treatment with 17β-estradiol also reduced the PAOX protein levels. Treatment with selective ESR antagonists and knockdown of ESR members revealed that estrogen receptor 2 (ESR2; also known as ERβ) was responsible for the repression of PAOX by 17β-estradiol. A luciferase reporter assay showed that 17β-estradiol downregulates PAOX promoter activity and that 17β-estradiol-dependent PAOX repression disappeared after deletions (−3126/−2730 and −1271/−1099 regions) or mutations of activator protein 1 (AP-1) binding sites in the PAOX promoter. Chromatin immunoprecipitation analysis showed that ESR2 interacts with AP-1 bound to each of the two AP-1 binding sites. These results demonstrate that 17β-estradiol represses PAOX transcription by the interaction of ESR2 with AP-1 bound to the PAOX promoter. This suggests that estrogen deficiency may upregulate PAOX expression and decrease polyamine levels. Full article
(This article belongs to the Special Issue The Role of Estrogen Receptors in Health and Disease 2.0)
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Review

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17 pages, 637 KiB  
Review
Estrogen Receptors Mediated Negative Effects of Estrogens and Xenoestrogens in Teleost Fishes—Review
by Konrad Wojnarowski, Paulina Cholewińska, Dušan Palić, Małgorzata Bednarska, Magdalena Jarosz and Iga Wiśniewska
Int. J. Mol. Sci. 2022, 23(5), 2605; https://doi.org/10.3390/ijms23052605 - 26 Feb 2022
Cited by 17 | Viewed by 4094
Abstract
Estrogen receptors (ERs) play a key role in many biochemical and physiological processes, that are involved in maintaining organism homeostasis. At the most basic level, they can be divided into nuclear estrogen receptors and membrane estrogen receptors that imply their effect in two [...] Read more.
Estrogen receptors (ERs) play a key role in many biochemical and physiological processes, that are involved in maintaining organism homeostasis. At the most basic level, they can be divided into nuclear estrogen receptors and membrane estrogen receptors that imply their effect in two ways: slower genomic, and faster non-genomic. In these ways, estrogens and xenoestrogens can negatively affect animal health and welfare. Most of the available literature focuses on human and mammalian physiology, and clearly, we can observe a need for further research focusing on complex mutual interactions between different estrogens and xenoestrogens in aquatic animals, primarily fishes. Understanding the mechanisms of action of estrogenic compounds on the ERs in fishes and their negative consequences, may improve efforts in environmental protection of these animals and their environment and benefit society in return. In this review, we have summarized the ER-mediated effects of xenoestrogens and estrogens on teleost fishes metabolism, their carcinogenic potential, immune, circulatory, and reproductive systems. Full article
(This article belongs to the Special Issue The Role of Estrogen Receptors in Health and Disease 2.0)
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