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Steroid Receptor Coactivator-2 Regulated Transcriptome in Human Endometrial Stromal Cells

ABSTRACT: RNA-sequencing of mRNA isolated from in vitro decidualizaing human endometrial stromal cells with or without siRNA-mediated knockdown of steroid receptor coactivator-2/nuclear receptor coactivator 2 (SRC-2/NCOA2)

ORGANISM(S): Homo sapiens

PROVIDER: GSE121584 | GEO | 2018/10/23

REPOSITORIES: GEO

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Steroid Receptor Coactivator-2 Regulated Transcriptome in Human Endometrial Stromal Cells

Project description:Steroid Receptor Coactivator-2 Regulated Transcriptome in Human Endometrial Stromal Cells

| PRJNA497833 | ENA

Steroid Receptor Coactivator-2 Drives Epithelial Reprogramming That Enalbles Murine Embryo Implantation

Project description:Using conditional knockout technology, we demonstrate that steroid receptor coactivator-2 (SRC-2) is essential for development of the receptive uterus for embryo implantation. Through bulk RNA-seq analysis, we reveal that endometrial SRC-2 is required for not only the induction of the expression of established genes associated with uterine receptivity but also for the expression of genes involved in endometrial epithelial changes that enable attachment and invasion of the embryo into the underlying stroma. Together, these RNA-seq results underscore the importance of SRC-2 as a transcriptional coregulator in the endometrium during the periimplantation period.

2023-11-20 | GSE237740 | GEO

Genome-wide Profiling of Steroid Receptor Coactivator 2 in mouse liver

Project description:Steroid Receptor 2 (SRC-2) is a coactivator involved in hepatic metabolism. To better understand its temporal involvement in metabolism genome wide profiling was performed at 2 time ZT4 and ZT18 as well as in the SRC-2 knockout mouse.

2014-11-10 | GSE53039 | GEO

Tissue- and Pathway-Specific Metabolomic Profiles of the Steroid Receptor Coactivator (SRC) family

Project description:The rapidly growing family of coregulators of nuclear receptors includes coactivators that promote transcription and corepressors that harbor the opposing function. In recent years, coregulators have begun to emerge as important regulators of metabolic homeostasis, including the p160 Steroid Receptor Coactivator (SRC) family. Members of the SRC family have been ascribed important roles in control of gluconeogenesis in liver and fatty acid oxidation in skeletal muscle. To provide a deeper and more granular understanding of the metabolic impact of SRC family members, we have performed targeted metabolomics analysis of key metabolic byproducts of glucose, fatty acid, and amino acid metabolism in mice with global knockout of SRC-1, SRC-2, or SRC-3. We measured amino acids, acyl carnitines, and organic acids in five tissues with key metabolic functions (liver, heart, skeletal muscle, brain, plasma) isolated from SRC-1, -2, or -3 knockout mice and their wild-type littermates in the fed and fasted conditions, thereby unveiling unique metabolic functions of each SRC coactivator. Overall, we observed entire groups or subgroups of metabolites belonging to discrete metabolic pathways that were influenced in different tissues and/or feeding states due to ablation of individual SRC isoforms. Surprisingly, we identified very few metabolites that changed universally across the three SRC knockout models. These findings demonstrate that coactivator function has very limited redundancy even within the homologous SRC coactivator family. Furthermore, this work also demonstrates the use of metabolomics as a means for identifying novel metabolic regulatory functions of transcriptional coregulators.

2013-04-10 | MTBLS30 | MetaboLights

SRC-2/NCOA genomic binding in decidualizing human endometrial stromal cells

Project description:Whole genome binding profile of SRC-2/NCOA2 in human endometrial stromal cells

2018-12-04 | GSE123246 | GEO

Regulation of pathogenic T helper 17 cell differentiation by steroid receptor coactivator-3

Project description:T helper 17 (Th17) cell development is programmed by the orphan nuclear receptor RORgt, but the underlying mechanism is not well understood. Nuclear receptor-mediated transcriptional activation depends on coactivators. Here we show that the steroid receptor coactivator-3 (SRC-3) critically regulates Th17 cell differentiation. Reduced incidence of experimental autoimmune encephalitis (EAE) associated with decreased Th17 cell generation in vivo was observed in mice with SRC-3 deletion specifically in T cells. In vitro, SRC-3 deficiency did not affect TGF-/IL-6-induced Th17 cell generation but severely impaired pathogenic Th17 differentiation induced by IL-1/IL-6/IL-23. Microarrays were used to showed that SRC-3 not only regulates IL-17A but also IL-1R1 expression. SRC-3 bound to Il17a and Il1r1 loci in a RORtdependent manner and was required for recruitment of the p300 acetyltransferase. Thus, SRC-3 is critical in RORt-dependent gene expression during Th17 cell-driven autoimmune diseases.

2018-05-02 | GSE113927 | GEO

A Steroid Receptor Coactivator Stimulator (MCB-613) Prevents Adverse Remodeling After Myocardial Infarction

Project description:A Steroid Receptor Coactivator Stimulator (MCB-613) Prevents Adverse Remodeling After Myocardial Infarction

2020-09-06 | GSE157542 | GEO

A SRC-3 gene signature in predecidual T-HESC

Project description:Steroid Receptor Coactivator-3 (SRC-3) knockdown in human endometrial stromal cells (HESCs) blocks their decidualization. This result provides translational support for recent studies in the mouse in which conditional SRC-3 knockout in progesterone receptor-positive cells of the endometrium results in early pregnancy loss due to a defect in normal decidualization. RNAseq was performed on the telomerase-immortalised endometrial stromal cell line T-HESC (CRL-4003; American Type Culture Collection) with or without SRC-3 knockdown to identify the transcriptome that is dependent on SRC-3 prior to hormone-dependent HESC decidualization.

2022-11-15 | GSE210936 | GEO

Steroid nuclear receptor coactivator 2 controls immune tolerance by promoting induced Treg differentiation via upregulating Nr4a2

Project description:Purpose:Steroid nuclear receptor coactivator 2 (SRC2) is a member of family of transcription co-activators. While SRC1 inhibits the differentiation of regulatory T cells (Tregs) critical for establishing immune tolerance, we show here that SRC2 stimulates Treg differentiation. SRC2 is dispensable for the development of thymic Tregs, whereas naïve CD4+ T cells from mice deficient of SRC2 specific in Tregs (SRC2fl/fl/Foxp3YFP-Cre) display defective Treg differentiation. Furthermore, the aged SRC2fl/fl/Foxp3YFP-Cre mice spontaneously develop autoimmune phenotypes including enlarged spleen and lung inflammation infiltrated with IFNγ-producing CD4+ T cells. SRC2fl/fl/Foxp3YFP-Cre mice also develop severer experimental autoimmune encephalomyelitis (EAE) due to reduced Tregs. Mechanically, SRC2 recruited by NFAT1 binds to the promoter and activates the expression of Nr4a2 which then stimulates Foxp3 expression to promote Treg differentiation. Members of SRC family co-activators thus play distinct roles in Treg differentiation and are potential drug targets for controlling immune tolerance

2022-04-30 | GSE201431 | GEO

Endometrial gland impacts on stromal cell decidualization

Project description:Uterine glands and, by inference, their secretions impact uterine receptivity, blastocyst implantation, stromal cell decidualization, and placental development. Changes in gland function across the menstrual cycle are impacted by steroid hormones, estrogen and progesterone, as well as stroma-derived factors. Using an endometrial epithelial organoid (EEO) system, transcriptome and proteome analyses identified distinct responses of the EEO to steroid hormones and prostaglandin E2 (PGE2). Notably, steroid hormones and PGE2 modulated the basolateral secretion of EEO proteins, where cystatin C (CST3) was significantly increased by progesterone and PGE2. CST3 treatment of decidualizing stromal cells significantly decreased the decidualization markers PRL and IGFBP1. The attenuation of stromal cell decidualization via CST3 suggests a role for uterine gland-derived proteins in controlling the extent of decidualization. These findings provide evidence that uterine gland-derived factors directly impact stromal cell decidualization, which has strong implications for better understanding pregnancy establishment and female fertility in humans.

2023-10-11 | PXD034357 | Pride

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