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Cells
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Estrogen Receptor Hormone Action
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Estrogen Receptor Hormone Action

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Signaling".

Deadline for manuscript submissions: closed (30 September 2021) | Viewed by 10766

Special Issue Editor

Dr. Ratna K. Vadlamudi

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Guest Editor
Mays Cancer Center, San Antonio, TX, USA

Special Issue Information

Dear Colleagues,

The estrogen receptor (ER) is a ligand-dependent transcription factor that modulates the transcription of numerous genes and is implicated in the progression of hormone-responsive cancers and diseases. Accumulating evidence suggests that the ER signalosome involves two distinct ERs (ERα or ERβ), multiple ER-coregulator proteins, and demonstrates activity in both ER-genomic functions and ER cytoplasmic/membrane-mediated signalling events (non-genomic signalling). With the advent genome-wide analysis, researchers have identified the existence of ER fusion proteins, isoforms, new target genes, and ER mutations during pathogenesis. Therefore, understanding the complexity of ER hormone actions, ER signalling pathways, and the biological implications of these signalling events is crucial to devise and develop novel treatment modalities. This Special Issue is focused on understanding the current status of the field in ER hormone signalling. This edition will analyze reviews and original papers covering a wide range of topics related to the mechanisms of estrogen signalling, including: ERα and β, ER mutations, ER coregulators, ER genome-wide studies, novel ER agonists and ER antagonists/SERDs, and the pathological effects of ER hormone signalling on uterine biology, endometriosis, inflammation, stroke, neuronal diseases, cancer, and other related topics.

Dr. Ratna K. Vadlamudi
Guest Editor

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Keywords

  • Estrogen receptor hormone signalling
  • Estrogen receptors alpha and beta
  • Estrogen signalling and cancer
  • Estrogen signalling and neuronal diseases
  • Estrogen receptor agonists and antagonists
  • Estrogen signalling on uterine biology

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Published Papers (2 papers)

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Research

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13 pages, 2397 KiB  
Article
DHEA Protects Human Cholangiocytes and Hepatocytes against Apoptosis and Oxidative Stress
by Ewa Kilanczyk, Dagmara Ruminkiewicz, Jesus M. Banales, Piotr Milkiewicz and Małgorzata Milkiewicz
Cells 2022, 11(6), 1038; https://doi.org/10.3390/cells11061038 - 18 Mar 2022
Cited by 9 | Viewed by 3081
Abstract
Primary biliary cholangitis (PBC) is a rare chronic cholestatic and immune-mediated liver disease of unknown aetiology that targets intrahepatic bile duct cells (cholangiocytes) and primarily affects postmenopausal women, when their estrogen levels sharply decrease. An impaired cholangiocyte response to estrogen characterizes the terminal [...] Read more.
Primary biliary cholangitis (PBC) is a rare chronic cholestatic and immune-mediated liver disease of unknown aetiology that targets intrahepatic bile duct cells (cholangiocytes) and primarily affects postmenopausal women, when their estrogen levels sharply decrease. An impaired cholangiocyte response to estrogen characterizes the terminal stage of the disease, as this is when an inefficiency of cholangiocyte proliferation, in balancing the loss of intrahepatic bile ducts, is observed. Here, we report that the estrogen precursor dehydroepiandrosterone (DHEA) and its sulfate metabolites, DHEA-S and 17 β-estradiol, enhance the proliferation of cholangiocytes and hepatocytes in vitro. Flow cytometry analysis showed that DHEA and DHEA-S decreased glyco-chenodeoxycholic acid (GCDC)-driven apoptosis in cholangiocytes. Cell viability assay (MTT) indicated that ER-α, -β, and the G-protein-coupled estrogen receptor, are involved in the protection of DHEA against oxidative stress in cholangiocytes. Finally, immunoblot analysis showed an elevated level of steroid sulfatase and a reduced level of sulfotransferase 1E1 enzymes, involved in the desulfation/sulfation process of estrogens in cirrhotic PBC, and primary sclerosis cholangitis (PSC) liver tissues, another type of chronic cholestatic and immune-mediated liver disease. Taken together, these results suggest that DHEA can prevent the deleterious effects of certain potentially toxic bile acids and reactive oxygen species, delaying the onset of liver disease. Full article
(This article belongs to the Special Issue Estrogen Receptor Hormone Action)
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Review

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13 pages, 1227 KiB  
Review
Estrogen Receptors in Polycystic Ovary Syndrome
by Xue-Ling Xu, Shou-Long Deng, Zheng-Xing Lian and Kun Yu
Cells 2021, 10(2), 459; https://doi.org/10.3390/cells10020459 - 21 Feb 2021
Cited by 47 | Viewed by 7109
Abstract
Female infertility is mainly caused by ovulation disorders, which affect female reproduction and pregnancy worldwide, with polycystic ovary syndrome (PCOS) being the most prevalent of these. PCOS is a frequent endocrine disease that is associated with abnormal function of the female sex hormone [...] Read more.
Female infertility is mainly caused by ovulation disorders, which affect female reproduction and pregnancy worldwide, with polycystic ovary syndrome (PCOS) being the most prevalent of these. PCOS is a frequent endocrine disease that is associated with abnormal function of the female sex hormone estrogen and estrogen receptors (ERs). Estrogens mediate genomic effects through ERα and ERβ in target tissues. The G-protein-coupled estrogen receptor (GPER) has recently been described as mediating the non-genomic signaling of estrogen. Changes in estrogen receptor signaling pathways affect cellular activities, such as ovulation; cell cycle phase; and cell proliferation, migration, and invasion. Over the years, some selective estrogen receptor modulators (SERMs) have made substantial strides in clinical applications for subfertility with PCOS, such as tamoxifen and clomiphene, however the role of ER in PCOS still needs to be understood. This article focuses on the recent progress in PCOS caused by the abnormal expression of estrogen and ERs in the ovaries and uterus, and the clinical application of related targeted small-molecule drugs. Full article
(This article belongs to the Special Issue Estrogen Receptor Hormone Action)
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