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ATAC-seq datasets for chromatin accessibility quantification during decidualization in mice

ABSTRACT: ATAC-seq datasets for chromatin accessibility quantification during decidualization in mice

PROVIDER: PRJNA1018849 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26109104_1.fastq.gz	Fastqsanger.gz
	SRR26109104_2.fastq.gz	Fastqsanger.gz
	SRR26109105_1.fastq.gz	Fastqsanger.gz
	SRR26109105_2.fastq.gz	Fastqsanger.gz
	SRR26109106_1.fastq.gz	Fastqsanger.gz

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ATAC-seq datasets for chromatin accessibility quantification during decidualization in mice

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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.

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cAMP/PKA signaling promotes AKT deactivation via reducing CIP2A expression, thereby facilitating decidualization

Project description:Decidualization is a progesterone-initiated differentiation concerning the endometrium and is dedicated to supporting the placenta and embryo development. During the process, cAMP signaling is widely known to be indispensable, but the details are not fully understood. In this study, we show that cAMP signaling promotes AKT deactivation in endometrial stromal cells, which favors their decidualization. The deactivation of AKT is found to be a consequence of the reduced expression of several inhibitors of PP2A, the major phosphatase of AKT, with CIP2A being the most prominent. To show that CIP2A loss is obligatory for decidualization, we performed this ATAC-seq analysis. Persistent CIP2A expression impairs the chromatin accesibility remodeling during decidualization.

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