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SCGB2A1 deficiency impairs endometrial stromal cell decidualization by decreasing CDK3-mediated proliferation in patients with recurrent implantation failure

ABSTRACT: SCGB2A1 deficiency impairs endometrial stromal cell decidualization by decreasing CDK3-mediated proliferation in patients with recurrent implantation failure

PROVIDER: PRJNA1121401 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29325504_1.fastq.gz	Fastqsanger.gz
	SRR29325504_2.fastq.gz	Fastqsanger.gz
	SRR29325505_1.fastq.gz	Fastqsanger.gz
	SRR29325505_2.fastq.gz	Fastqsanger.gz
	SRR29325506_1.fastq.gz	Fastqsanger.gz

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SCGB2A1 deficiency impairs endometrial stromal cell decidualization by decreasing CDK3-mediated proliferation in patients with recurrent implantation failure

Project description:Recurrent implantation failure (RIF) presents a significant challenge in the field of assisted reproductive technology, primarily stemming from compromised decidualization that impacts endometrial receptivity. Despite ongoing research efforts, the comprehensive molecular regulatory mechanisms involved in RIF remain incompletely understood. This study revealed significantly reduced levels of secretoglobin, family 2A, member 1 (SCGB2A1) in both the mid-secretory endometrium and uterine fluid of RIF patients compared to control subjects. Besides, combined with RNA sequencing results, we demonstrated that the suppression of SCGB2A1 results in reduced cell proliferation and impaired decidualization by modulating CDK3 signaling during cell cycle transition in immortalized human endometrial stromal cells (T-HESCs) and primary HESCs. Furthermore, our findings indicated that inhibition of endometrial SCGB2A1 in a rat model hinders embryo implantation and disrupts decidualization. In conclusion, this study provides evidence that SCGB2A1 serves as a novel biomarker for endometrial receptivity and plays a crucial role in the regulation of human endometrial decidualization. The findings offer valuable insights into the pathogenesis of decidualization-related RIF and have the potential to enhance strategies for improving pregnancy outcomes.

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Project description:Proper decidualization is vital in preparation for a potential embryo receptivity, placentation, menstrual health and subsequent endometrial regeneration. Given the importance of extracellular vesicles (EVs) in intercellular communication, and recently in embryo implantation and indicators of menstrual cycle and fertility, we investigated their role during decidualization. Overall, this study provides an insight into distinct variation in sEV composition depending upon the level of decidualization of endometrial stromal cells, with the signaling potential to coordinate endometrial health ranging from embryo implantation, facilitating placentation and subsequent endometrial regeneration.

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Project description:We aimed to identify altered biological processes in the endometrium that may be potential markers of receptive endometrium. RNA expression profiling of the endometrium during the window of implantation was performed in patients with Recurrent Implantation Failure (RIF) versus fertile controls.

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Project description:Transcriptomic studies have identified gene expression profiles characteristic of the window of implantation and preliminary studies have indicated that these may be disrupted in some women with recurrent implantation failure (RIF). The aims of this study were to elucidate how the endometrial gene expression profile differs between women with RIF and controls, and to investigate whether a predictor set of genes could be identified able to distinguish between these women.

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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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Project description:Recurrent implantation failure(RIF) is an urgent problem to be solved in reproduction.Currently, endometrium decidualization damage is considered as one of the important causes, but the mechanism is still unclear. Prokineticin 2(PK2) is a newly discovered secreted protein with multiple biological functions, and its role in the endometrium is unknown.Our previous study showed that PK2 was significantly increased in RIF patients, but endometrial decidualization markers PRL and IGFBP1 were lower compared with the control group. We performed transcriptome sequencing, we found there were significant differences between the PK2 overexpression group and the control group. Differential genes mainly involved in decidualization process including adhesion, immunity, chemotaxis, ect.

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