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

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

PROVIDER: PRJNA600488 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10869364.fastq.gz	Fastqsanger.gz
	SRR10869365.fastq.gz	Fastqsanger.gz
	SRR10869366.fastq.gz	Fastqsanger.gz
	SRR10869367.fastq.gz	Fastqsanger.gz
	SRR10869369.fastq.gz	Fastqsanger.gz

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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 [RNAseq]

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

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

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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.

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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.

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

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IFN-kappa inhibits HPV31 transcription by inducing Sp100 proteins

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