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GPER1 inhibits placental type I IFN responses to preserve fetal health during maternal infection [RNAseq]

ABSTRACT: Inhibition of GPER1 in pregnant mice significantly alters inflammation and angiogenesis in the placenta, but does not significantly impact the lung

ORGANISM(S): Mus musculus

PROVIDER: GSE143431 | GEO | 2021/01/14

REPOSITORIES: GEO

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GPER1 inhibits placental type I IFN responses to preserve fetal health during maternal infection

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

2021-01-14 | GSE143432 | GEO

GPER1 inhibits placental type I IFN responses to preserve fetal health during maternal infection

Project description:GPER1 inhibits placental type I IFN responses to preserve fetal health during maternal infection

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GPER1 inhibits placental type I IFN responses to preserve fetal health during maternal infection [GECKOscreen]

Project description:Identification of factors that control ifn responses during pregnancy

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GPER1 inhibits placental type I IFN responses to preserve fetal health during maternal infection [RNAseq]

Project description:GPER1 inhibits placental type I IFN responses to preserve fetal health during maternal infection [RNAseq]

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GPER1 inhibits placental type I IFN responses to preserve fetal health during maternal infection [GECKOscreen]

Project description:GPER1 inhibits placental type I IFN responses to preserve fetal health during maternal infection [GECKOscreen]

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Proteomic identification of the GPER1 interactome

Project description:The G-protein coupled estrogen receptor GPER1 is thought to mediate rapid estrogen signaling at the membrane. Despite considerable efforts over the last years, its physiological ligand(s), interactors, and regulators are still very poorly understood. This is particularly problematic at a time when the inducibility of GPER1 activity has been challenged. We therefore investigated both activity and interactome of GPER1. We could confirm that GPER1 can behave as a constitutivley active signaling protein. Using proximity labelling and immunoprecipitation coupled to mass spectrometry, we explored the GPER1 interactome. Intersecting the results of the two proteomic approaches and validating some candidate interactors, we generate a GPER1 a resource, which may be useful for further functional studies in the future.

2023-11-06 | PXD041943 | Pride

Activation of GPER1 in macrophage ameliorates UUO-induced renal fibrosis

Project description:Numerous studies have proven the critical role of macrophages in the renal fibrosis process. Notably, G Protein-coupled Estrogen Receptor 1 (GPER1), a novel estrogen receptor, has been shown to play a ubiquitous role in the regulation of macrophage activities and proinflammatory pathways. However, the precise role of GPER1 in macrophage-mediated renal fibrosis is unknown. In this study, we aimed to investigate the function of macrophage GPER1 in the UUO-induced renal fibrosis model. Compared to vehicle-treated ovariectomized (OVX) female and male UUO models, we observed that G-1 (GPER1 agonist)-treated OVX female and male UUO mice had fewer renal fibrotic lesions and less M1 and M2 macrophage infiltration in the kidney tissues. Conversely, Gper1 deletion in male UUO mice accelerated renal fibrosis and increased inflammation. In vitro studies also revealed that GPER1 activation reduced M0 macrophage polarization towards M1 and M2 phenotypes. The RNA sequencing analysis and immunoblotting indicated that GPER1 activation was primarily involved in downregulating immune pathways activation and inactivating MAPK pathways. Tubular epithelial cells co-cultured with G1-pretreated M1 macrophages exhibited fewer injuries and immune activation. In addition, fibroblasts co-cultured with G1-pretreated M2 macrophages showed downregulated extracellular matrix expression. Overall, this is the first study to demonstrate the effect of GPER1 on macrophage-mediated renal fibrosis via inhibition of M1 and M2 macrophage polarization. These findings indicate that GPER1 may be a promising therapeutic target for the treatment of renal fibrosis.

2023-12-20 | GSE235718 | GEO

Estrogen sensing by GPER1 activates PI3K/mTOR to promote gender dimorphism in liver growth and cancer

Project description:Liver cancer is a common cause of cancer death, with a male-predominant incidence due, in part, to increased estrogen levels in cirrhotic patients. It is unknown, however, how estrogen is sensed to influence this process. Here, we show that estrogen activates the G protein-coupled estrogen receptor 1 (GPER1), expressed in hepatocytes, to enhancing hepatocyte size, cell cycle progression and cell proliferation, thereby increasing liver growth in zebrafish larvae and adults. GPER1 stimulation activates PI3K/mTOR signaling, and mTOR is essential for both normal and regenerative organ growth. Genetic loss of GPER1 diminishes and estrogen exposure accelerates chemical carcinogenesis, specifically in males. Chemical inhibition of GPER1 significantly reduces cancer incidence and progression in a gender-specific fashion. Our studies identify GPER1 as a hepatic estrogen sensor that mediates gender dimorphic growth, mTOR activation, and can serve as a therapeutic target for liver cancer treatment.

2019-05-29 | GSE92544 | GEO

Effect of Genetically Reduced Maternal Myostatin on Late Gestation Maternal, Fetal, and Placental Metabolomes in Mice.

Project description:Myostatin (gene symbol: Mstn) is an autocrine and paracrine inhibitor of muscle growth. Pregnant mice with genetically reduced levels of myostatin give birth to offspring with greater adult muscle mass and bone biomechanical strength. However, maternal myostatin is not detectable in fetal circulations. Fetal growth is dependent on the maternal environment, and the provisioning of nutrients and growth factors by the placenta. Thus, this study examined the effect of reduced maternal myostatin on maternal and fetal serum metabolomes, as well as the placental metabolome. Fetal and maternal serum metabolomes were highly distinct, which is consistent with the role of the placenta in creating a specific fetal nutrient environment. There was no effect from myostatin on maternal glucose tolerance or fasting insulin. In comparisons between pregnant control and Mstn+/- mice, there were more significantly different metabolite concentrations in fetal serum, at 50, than in the mother's serum at 33, confirming the effect of maternal myostatin reduction on the fetal metabolic milieu. Polyamines, lysophospholipids, fatty acid oxidation, and vitamin C, in fetal serum, were all affected by maternal myostatin reduction.

2023-06-08 | MTBLS3345 | MetaboLights

Transcription profiling of mouse developing placenta, with placental and decidual tissues profiled separately

Project description:We used full genome microarrays to profile the full lifetime of the mouse placenta from embryonic day 8.5 (e8.5), at the time of chorioallantoic fusion, until postnatal day 0 (P0). At each stage, the fetal placenta and maternal decidual tissues were dissected and profiled separately Experiment Overall Design: Mouse placentas were obtained from timed pregnant female mice at each timepoint, and fetal tissues were used to confirm embryo staging. Fetal placenta and maternal decidual tissues were dissected and pooled separately for each litter prior to RNA extraction and hybridization on Affymetrix microarrays.

2008-06-11 | E-GEOD-11220 | biostudies-arrayexpress

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