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

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

PROVIDER: PRJNA1024993 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26313759.fastq.gz	Fastqsanger.gz
	SRR26313760.fastq.gz	Fastqsanger.gz
	SRR26313761.fastq.gz	Fastqsanger.gz
	SRR26313762.fastq.gz	Fastqsanger.gz
	SRR26313763.fastq.gz	Fastqsanger.gz

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Similar Datasets

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

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-05-10 | GSE244843 | 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

Relaxin reverses inflammatory and immune signals in aged hearts

Project description:Background: ‘Healthy’ aging drives structural and functional changes in the heart including maladaptive electrical remodeling, fibrosis and inflammation, which lower the threshold for cardiovascular diseases such as heart failure (HF) and atrial fibrillation (AF). Despite mixed results in recent clinical trials, Relaxin-therapy for 2-days could reduce mortality by 37% at 180-days post-treatment, in patients with acute decompensated HF. Relaxin’s short life-span (hours) but long-lasting protective actions led us to test the hypothesis that relaxin acts at a genomic level to reverse maladaptive remodeling in aging and HF. Methods and Results: Young (9-month) and aged (24-month), male and female F-344/Brown Norway rats were treated with relaxin (0.4 mg/kg/day) for 2-weeks delivered by subcutaneous osmotic mini-pumps or with sodium acetate (controls). The genomic effects of aging and relaxin were evaluated by extracting RNA from the left ventricles and analyzing genomic changes by RNA-sequencing, Ingenuity Pathway Analysis, MetaCore and tissue immunohistochemistry. We found that aging promotes a native inflammatory response with distinct sex-differences and relaxin suppresses transcription of multiple genes and signaling pathways associated with inflammation and HF in both genders. In addition, aging significantly increased macrophage infiltration in the ventricles and activation of the complement cascade, and relaxin reversed these age-related effects. Conclusion: These data support the hypothesis that relaxin alters gene transcription and suppresses inflammatory pathways and genes associated with HF and aging. Relaxin’s suppression of inflammation and fibrosis supports its potential as a therapy for cardiovascular and inflammation-related diseases, such as HF, AF and diabetes.

2018-01-04 | GSE106377 | GEO

Expression profiling in OVCAR8 cells following treatment with relaxin-2 (RLN2)

Project description:The relaxin-RXFP1 signaling loop promotes survival and proliferation in a panel of high-grade serous ovarian (HGSOC) cancer cell lines. Knockdown of either the relaxin receptor-1(RXFP1) or relaxin-2 (RLN2) decreased growth and tumorigenicity and increased apoptosis in dependent HGSOC cell lines. Transcriptome profiling of relaxin-dependent HGSOC cells using RNA-Seq revealed genes with altered expression levels following relaxin treatment. This included components of the Notch signaling pathway (NOTCH1 and NOTCH3), Wnt signaling (DVL1, LRP5, BCL9) and extracellular matrix regulation (VEGF-A, MMP9, MMP23). Collectively, genes and pathways upregulated by relaxin provide insight into the mechanisms by which it sustains proliferation of dependent cells.

2020-12-31 | GSE151280 | GEO

Development of Pathway Preferential Estrogens Affording Beneficial Metabolic and Vascular Actions without Reproductive Tissue Stimulation in Mice

Project description:There is great medical need for estrogens having favorable pharmacological profiles, supporting desirable activities for menopausal women such as metabolic and vascular protection but lacking stimulatory activities on the breast or uterus. Here, we report the development of structurally novel estrogens with favorable target tissue-selective estrogenic activity. Through a process of structural alteration of the hormone estradiol that preserves essential chemical and physical features of estradiol but greatly moderates its binding affinity for the estrogen receptors (ERs), we obtained Pathway Preferential Estrogens (PaPEs) capable of having interaction with ER that is sufficient to activate the extranuclear-initiated signaling pathway preferentially over the direct nuclear-initiated pathway. PaPE modulate a pattern of gene regulation and cellular and biological processes that result in essentially no stimulation of reproductive and mammary tissues and breast cancer cells, but have a favorable pattern of activity on metabolic tissues and the vasculature. The structural permutation process represents a novel approach to govern the balance in utilization of extranuclear vs. nuclear pathways of ER action to obtain tissue-selective/non-nuclear pathway-preferential estrogens, which should prove to be beneficial for postmenopausal hormone replacement. The approach may also have broad applicability for other members of the nuclear hormone receptor superfamily.

2016-07-20 | GSE73663 | GEO

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