Egr1 is rapidly and transiently induced by estrogen and bisphenol A via activation of nuclear estrogen receptor-dependent ERK1/2 pathway in the uterus

Kim, Hye Ryun; Kim, Yeon Sun; Yoon, Jung Ah; Lyu, Sang Woo; Shin, Hyejin; Lim, Hyunjung Jade; Hong, Seok‐Ho; Lee, Dong Ryul; Song, Haengseok

doi:10.1016/j.reprotox.2014.10.010

Cited by 46 publications

(36 citation statements)

References 38 publications

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“…A possibility to explain such sex differences in EGR1 expression could reside in the ovarian hormone estrogen, as the latter can directly up-regulate EGR1 expression. In the mouse mammary gland, for instance, EGR1 is at the center of a gene regulation network triggered by exposure to estrogen (Lu et al, 2008), while its mRNA levels in the mouse uterus are up-regulated following estrogen treatment (Kim et al, 2014). Surprisingly, although an estrogen response element (ERE) has been identified on the Egr1 promoter, the induction of Egr1 transcription by estrogen is mediated by SRF and Elk1 binding to SRE rather than binding of estrogen receptors to their ERE, and is blocked by a MAPK but not PI3K pathway inhibitor in rat cardiomyocytes or MCF-7 human breast cancer cells (Slade and Carter, 2000; Chen et al, 2004), indicating that EGR1 is a downstream target of estrogen’s non-genomic effects.…”

Section: Functions and Regulations Of Egr1mentioning

confidence: 99%

“…Surprisingly, although an estrogen response element (ERE) has been identified on the Egr1 promoter, the induction of Egr1 transcription by estrogen is mediated by SRF and Elk1 binding to SRE rather than binding of estrogen receptors to their ERE, and is blocked by a MAPK but not PI3K pathway inhibitor in rat cardiomyocytes or MCF-7 human breast cancer cells (Slade and Carter, 2000; Chen et al, 2004), indicating that EGR1 is a downstream target of estrogen’s non-genomic effects. Interestingly, treatment with progesterone either doesn’t affect Egr1 mRNA (Lu et al, 2008), or dampens the estrogen-induced up-regulation of Egr1 mRNA in the mouse uterus (Kim et al, 2014), which suggests that ovarian hormones can interact to regulate EGR1 expression. These interactions are likely to be specific to neurons, however, as Egr1, among other IEGs, is strongly up-regulated in Schwann cells following progesterone treatment (Mercier et al, 2001).…”

Section: Functions and Regulations Of Egr1mentioning

confidence: 99%

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The Role of Early Growth Response 1 (EGR1) in Brain Plasticity and Neuropsychiatric Disorders

Duclot

Kabbaj

2017

Front. Behav. Neurosci.

282

240

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It is now clearly established that complex interactions between genes and environment are involved in multiple aspects of neuropsychiatric disorders, from determining an individual’s vulnerability to onset, to influencing its response to therapeutic intervention. In this perspective, it appears crucial to better understand how the organism reacts to environmental stimuli and provide a coordinated and adapted response. In the central nervous system, neuronal plasticity and neurotransmission are among the major processes integrating such complex interactions between genes and environmental stimuli. In particular, immediate early genes (IEGs) are critical components of these interactions as they provide the molecular framework for a rapid and dynamic response to neuronal activity while opening the possibility for a lasting and sustained adaptation through regulation of the expression of a wide range of genes. As a result, IEGs have been tightly associated with neuronal activity as well as a variety of higher order processes within the central nervous system such as learning, memory and sensitivity to reward. The immediate early gene and transcription factor early growth response 1 (EGR1) has thus been revealed as a major mediator and regulator of synaptic plasticity and neuronal activity in both physiological and pathological conditions. In this review article, we will focus on the role of EGR1 in the central nervous system. First, we will summarize the different factors influencing its activity. Then, we will analyze the amount of data, including genome-wide, that has emerged in the recent years describing the wide variety of genes, pathways and biological functions regulated directly or indirectly by EGR1. We will thus be able to gain better insights into the mechanisms underlying EGR1’s functions in physiological neuronal activity. Finally, we will discuss and illustrate the role of EGR1 in pathological states with a particular interest in cognitive functions and neuropsychiatric disorders.

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Section: Functions and Regulations Of Egr1mentioning

confidence: 99%

Section: Functions and Regulations Of Egr1mentioning

confidence: 99%

The Role of Early Growth Response 1 (EGR1) in Brain Plasticity and Neuropsychiatric Disorders

Duclot

Kabbaj

2017

Front. Behav. Neurosci.

282

240

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“…In the late phase, E 2 facilitates epithelial cell (EC) proliferation. Recently, we demonstrated that Egr1 is rapidly and transiently induced in both ECs and stromal cells by E 2 via the nuclear estrogen receptor-a (ERa)-ERK1/2 pathway in the uterus (21). Furthermore, Egr1 has been shown to be specifically induced in subluminal stromal cells surrounding the implanted blastocyst (21,22).…”

mentioning

confidence: 99%

Estrogen induces EGR1 to fine‐tune its actions on uterine epithelium by controlling PR signaling for successful embryo implantation

Kim

Yoon

et al. 2018

FASEB j.

Self Cite

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The harmonized actions of ovarian E and progesterone (P) regulate the proliferation and differentiation of uterine cells in a spatiotemporal manner. Imbalances between these hormones often lead to infertility and gynecologic diseases. Whereas numerous factors that are involved in P signaling have been identified, few local factors that mediate E actions in the uterus have been revealed. Here, we demonstrate that estrogen induces the transcription factor, early growth response 1 ( Egr1), to fine-tune its actions in uterine epithelial cells (ECs) that are responsible for uterine receptivity for embryo implantation. In the presence of exogenous gonadotrophins, ovulation, fertilization, and embryonic development normally occur in Egr1 mice, but these animals experience the complete failure of embryo implantation with reduced artificial decidualization. Although serum levels of E and P were comparable between Egr1 and Egr1 mice on d 4 of pregnancy, aberrantly reduced levels of progesterone receptor in Egr1 uterine ECs caused enhanced E activity and impaired P response. Ultrastructural analyses revealed that Egr1 ECs are not fully able to provide proper uterine receptivity. Uterine mRNA landscapes in Egr1 mice revealed that EGR1 controls the expression of a subset of E-regulated genes. In addition, P signaling was unable to modulate estrogen actions, including those that are involved in cell-cycle progression, in ECs that were deficient in EGR1. Furthermore, primary coculture of Egr1 ECs with Egr1 stromal cells, and vice versa, supported the notion that Egr1 is required to modulate E actions on ECs to prepare the uterine environment for embryo implantation. In contrast to its role in ECs, loss of Egr1 in stroma significantly reduced stromal cell proliferation. Collectively, our results demonstrate that E induces EGR1 to streamline its actions for the preparation of uterine receptivity for embryo implantation in mice.-Kim, H.-R., Kim, Y. S., Yoon, J. A., Yang, S. C., Park, M., Seol, D.-W., Lyu, S. W., Jun, J. H., Lim, H. J., Lee, D. R., Song, H. Estrogen induces EGR1 to fine-tune its actions on uterine epithelium by controlling PR signaling for successful embryo implantation.

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“…The EGR1 motif was identified in the promoters of the PRDX5 and TXN genes. EGR1 is a well-known target of the estrogen receptor (ESR1);30 thus, we conjectured that ESR1 might mediate CES signaling, with consequent activation of the AML-1a and Elk1 transcription factors.…”

Section: Resultsmentioning

confidence: 99%

Chum salmon egg extracts induce upregulation of collagen type I and exert antioxidative effects on human dermal fibroblast cultures

Yoshino

Polouliakh

Meguro

et al. 2016

CIA

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Components of fish roe possess antioxidant and antiaging activities, making them potentially very beneficial natural resources. Here, we investigated chum salmon eggs (CSEs) as a source of active ingredients, including vitamins, unsaturated fatty acids, and proteins. We incubated human dermal fibroblast cultures for 48 hours with high and low concentrations of CSE extracts and analyzed changes in gene expression. Cells treated with CSE extract showed concentration-dependent upregulation of collagen type I genes and of multiple antioxidative genes, including OXR1, TXNRD1, and PRDX family genes. We further conducted in silico phylogenetic footprinting analysis of promoter regions. These results suggested that transcription factors such as acute myeloid leukemia-1a and cyclic adenosine monophosphate response element-binding protein may be involved in the observed upregulation of antioxidative genes. Our results support the idea that CSEs are strong candidate sources of antioxidant materials and cosmeceutically effective ingredients.

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Egr1 is rapidly and transiently induced by estrogen and bisphenol A via activation of nuclear estrogen receptor-dependent ERK1/2 pathway in the uterus

Cited by 46 publications

References 38 publications

The Role of Early Growth Response 1 (EGR1) in Brain Plasticity and Neuropsychiatric Disorders

The Role of Early Growth Response 1 (EGR1) in Brain Plasticity and Neuropsychiatric Disorders

Estrogen induces EGR1 to fine‐tune its actions on uterine epithelium by controlling PR signaling for successful embryo implantation

Chum salmon egg extracts induce upregulation of collagen type I and exert antioxidative effects on human dermal fibroblast cultures

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