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Endometrial gland impacts on stromal cell decidualization

ABSTRACT: Endometrial gland impacts on stromal cell decidualization

PROVIDER: PRJNA843696 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20733218_1.fastq.gz	Fastqsanger.gz
	SRR20733218_2.fastq.gz	Fastqsanger.gz
	SRR20733219_1.fastq.gz	Fastqsanger.gz
	SRR20733219_2.fastq.gz	Fastqsanger.gz
	SRR20733220_1.fastq.gz	Fastqsanger.gz

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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.

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Endometrial gland impacts on stromal cell decidualization

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Project description:The objectives of the present study were to determine whether obesity impacts human decidualization and the endometrial control of trophoblast invasion (both of which are required for embryo implantation) and evaluate the potential involvement of endometrial extracellular vesicles (EVs) in the regulation of these physiological processes. Using primary human cell cultures, we first demonstrated that obesity is associated with significantly lower in vitro decidualization of endometrial stromal cells (ESCs). We then showed that the trophoblastic cell line’s invasive ability was greater in the presence of conditioned media from cultures of ESCs from obese women. Using mass-spectrometry-based quantitative proteomics, we found that EVs isolated from uterine supernatants of biopsies from obese women (vs. nonobese women) presented a molecular signature focused on cell remodeling and angiogenesis. Lastly, the results of functional assays indicated that supplementation of the culture medium with EVs from nonobese women can rescue (at least in part) the defect in in vitro decidualization described in ESCs from obese women. Lastly, the addition of endometrial EVs from obese women (vs. nonobese women) was associated with significantly greater invasive activity by HTR-8/SVneo cells. In conclusion, our results provided new insights into the endometrial EVs’ pivotal role in the poor uterine receptivity observed in obese women.

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