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Relaxin Attenuates the Genomic Actions and Biological Effects of Estrogens in the Myometrium by Reducing Estrogen Receptor Alpha Phosphorylation

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE244843 | GEO | 2024/05/10

REPOSITORIES: GEO

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Relaxin Attenuates the Genomic Actions and Biological Effects of Estrogens in the Myometrium by Reducing Estrogen Receptor Alpha Phosphorylation [RNA-seq]

Project description:In this study we examine the extent and nature of functional interactions between the E2 and Rln signaling pathways in the myometrium. In addition, we delineate the mechanisms underlying functional interplay between the E2/ERα and Rln/RXFP1 signaling pathways at the molecular and physiological levels in myometrial tissue and cells during quiescence and contractility.

2024-05-10 | GSE244842 | GEO

Relaxin Attenuates the Genomic Actions and Biological Effects of Estrogens in the Myometrium by Reducing Estrogen Receptor Alpha Phosphorylation [ChIP-seq]

2024-05-10 | GSE244841 | GEO

Relaxin Attenuates the Genomic Actions and Biological Effects of Estrogens in the Myometrium by Reducing Estrogen Receptor Alpha Phosphorylation

Project description:Relaxin Attenuates the Genomic Actions and Biological Effects of Estrogens in the Myometrium by Reducing Estrogen Receptor Alpha Phosphorylation

| PRJNA1024993 | ENA

Relaxin Attenuates the Genomic Actions and Biological Effects of Estrogens in the Myometrium by Reducing Estrogen Receptor Alpha Phosphorylation [ChIP-seq]

Project description:Relaxin Attenuates the Genomic Actions and Biological Effects of Estrogens in the Myometrium by Reducing Estrogen Receptor Alpha Phosphorylation [ChIP-seq]

| PRJNA1024997 | ENA

Relaxin Attenuates the Genomic Actions and Biological Effects of Estrogens in the Myometrium by Reducing Estrogen Receptor Alpha Phosphorylation [RNA-seq]

Project description:Relaxin Attenuates the Genomic Actions and Biological Effects of Estrogens in the Myometrium by Reducing Estrogen Receptor Alpha Phosphorylation [RNA-seq]

| PRJNA1024999 | ENA

Relaxin Modulates the Genomic Actions and Biological Effects of Estrogen in the Myometrium [hTERT RNA-seq]

Project description:Estradiol (E2) and relaxin (Rln) are steroid and polypeptide hormones, respectively, with important roles in the female reproductive tract, including myometrium. Some actions of Rln, which are mediated by its membrane receptor RXFP1, require or are augmented by E2 signaling through its cognate nuclear steroid receptor, estrogen receptor alpha (ER⍺). In contrast, other actions of Rln act in opposition to the effects of E2. Here we explore the molecular and genomic mechanisms that underlie the functional interplay between E2 and Rln in the myometrium. We used both ovariectomized female mice and immortalized human myometrial cells expressing wild type or mutant ER⍺ (hTERT-HM-ER⍺ cells). Our results indicate that Rln attenuates the genomic actions and biological effects of estrogen in the myometrium and myometrial cells by reducing phosphorylation ER⍺ on serine 118 (S118). Interestingly, we observed a potent inhibitory effect of Rln on the E2-dependent binding of ER⍺ across the genome. The reduction in ER⍺ binding was associated with changes in the hormone-regulated transcriptome, including a decrease in the E2-dependent expression of neighboring genes. The inhibitory effects of Rln cotreatment on the E2-dependent phosphorylation of ER⍺ required the nuclear dual-specificity phosphatases DUSP1 and DUSP5. Moreover, the inhibitory effects of Rln were reflected in a concomitant inhibition of the E2-dependent contraction of myometrial cells. Collectively, our results identify a pathway that integrates Rln/RXFP1 and E2/ER⍺ signaling, resulting in a convergence of membrane and nuclear signaling pathways to control genomic and biological outcomes.

2024-08-31 | GSE275894 | GEO

Relaxin Modulates the Genomic Actions and Biological Effects of Estrogen in the Myometrium [hTERT RNA-seq]

Project description:Relaxin Modulates the Genomic Actions and Biological Effects of Estrogen in the Myometrium [hTERT RNA-seq]

| PRJNA1153523 | ENA

Physical Linkage of Estrogen Receptor α and Aromatase in Rat: Oligocrine and Endocrine Actions of CNS-Produced Estrogens.

Project description:Rapid-signaling membrane estrogen receptors (mERs) and aromatase (Aro) are present throughout the central nervous system (CNS), enabling acute regulation of CNS estrogenic signaling. We previously reported that spinal membrane Aro (mAro) and mERα oligomerize (1). As their organizational relationship would likely influence functions of locally produced estrogens, we quantified the mAro and mERα that are physically associated and nonassociated in two functionally different regions of rat CNS: the spinal cord, which has predominantly neural functionalities, and the hypothalamus, which has both neural and endocrine capabilities. Quantitative immunoprecipitation (IP), coimmunoprecipitation, and Western blot analysis were used to quantify the associated and nonassociated subpopulations of mAro and mERα. Regardless of estrous-cycle stage, virtually all mAro was oligomerized with mERα in the spinal cord, whereas only ∼15% was oligomerized in the hypothalamus. The predominance of nonassociated mAro in the hypothalamus, in combination with findings that many hypothalamic Aro-immunoreactive neurons could be retrogradely labeled with peripherally injected Fluoro-Gold, suggests that a portion of hypothalamic estrogens is secreted, potentially regulating pituitary function. Moreover, circulating estrogens increased hypothalamic Aro activity (quantified by the tritiated water-release assay) in the absence of increased Aro protein, revealing nongenomic regulation of Aro activity in the mammalian CNS. The demonstrated presence of associated and nonassociated mAro and mERα subpopulations in the CNS suggests that their selective targeting could restore impaired estrogen-dependent CNS functionalities while minimizing unwanted effects. The full physiological ramifications of brain-secreted estrogens remain to be explored.

| S-EPMC6692873 | biostudies-other

Estrogen receptor alpha isoform ERdelta7 in myometrium modulates uterine quiescence during pregnancy.

Project description:BackgroundCirculating estrogen (E2) levels are high throughout pregnancy and increase towards term, however its local tissue specific actions vary across gestation. For example, myometrial E2 regulated uterotonic action is disabled until term, whereas it's proliferative function is maintained in the breast. We have identified gestationally regulated splicing events, mediated by hnRNPG and modulated by E2 that generate alternatively spliced estrogen receptor alpha (ER?) variants (ER?7 and ER?46) in the myometrium. These variants allow for differential, gestationally regulated, modulation of the uterotonic action of E2.MethodsHuman myometrium isolated from preterm and term non-laboring and laboring pregnant women were analyzed for ER? isoforms and splice factor levels. Lentiviral mediated shRNA knockdown of hnRNPG and overexpression of ER?7 were performed in human myometrial (hTERT-HM) cells. Functional 3D collagen contraction assays were executed.FindingsER?7 acts as a dominant negative repressor of the uterotonic action of ER?66 and ER?46 isoforms through the regulation of the myometrial gap junction protein GJA1. Elimination of hnRNPG inhibits the generation of ER?7 while overexpression of ER?7 inhibited GJA1 expression. Moreover in vivo human myometrial hnRNPG levels decline at term in an E2 dependent manner resulting in a withdrawal of ER?7 levels and its tocolytic action at term.InterpretationOur findings implicate the unique role of ER?7 as a modulator of myometrial quiescence and define the mechanism of ER?7 generation, through hormonally regulated splicing events. FUND: This study was supported by NIH OPRU U01 supplement (HD047905), University of Pittsburgh and Wayne State University Perinatal Research Initiative (USA).

| S-EPMC6355643 | biostudies-literature

Anti-fibrotic actions of relaxin.

Project description:Fibrosis refers to the hardening or scarring of tissues that usually results from aberrant wound healing in response to organ injury, and its manifestations in various organs have collectively been estimated to contribute to around 45-50% of deaths in the Western world. Despite this, there is currently no effective cure for the tissue structural and functional damage induced by fibrosis-related disorders. Relaxin meets several criteria of an effective anti-fibrotic based on its specific ability to inhibit pro-fibrotic cytokine and/or growth factor-mediated, but not normal/unstimulated, fibroblast proliferation, differentiation and matrix production. Furthermore, relaxin augments matrix degradation through its ability to up-regulate the release and activation of various matrix-degrading matrix metalloproteinases and/or being able to down-regulate tissue inhibitor of metalloproteinase activity. Relaxin can also indirectly suppress fibrosis through its other well-known (anti-inflammatory, antioxidant, anti-hypertrophic, anti-apoptotic, angiogenic, wound healing and vasodilator) properties. This review will outline the organ-specific and general anti-fibrotic significance of exogenously administered relaxin and its mechanisms of action that have been documented in various non-reproductive organs such as the cardiovascular system, kidney, lung, liver, skin and tendons. In addition, it will outline the influence of sex on relaxin's anti-fibrotic actions, highlighting its potential as an emerging anti-fibrotic therapeutic.Linked articlesThis article is part of a themed section on Recent Progress in the Understanding of Relaxin Family Peptides and their Receptors. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v174.10/issuetoc.

| S-EPMC5406285 | biostudies-literature

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