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PARP-1/PARP-2 double deficiency results in recurrent early pregnancy loss and decidualization failure in mice

ABSTRACT: PARP-1/PARP-2 double deficiency results in recurrent early pregnancy loss and decidualization failure in mice

PROVIDER: PRJNA716989 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14061872.fastq.gz	Fastqsanger.gz
	SRR14061873.fastq.gz	Fastqsanger.gz
	SRR14061874.fastq.gz	Fastqsanger.gz
	SRR14061875.fastq.gz	Fastqsanger.gz
	SRR14061876.fastq.gz	Fastqsanger.gz

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PARP-1/PARP-2 double deficiency results in recurrent early pregnancy loss and decidualization failure in mice

Project description:Specifically, we found inhibition of PARP-1 and PARP-2 catalytic activity, or tissue-specific genetic knockout, results in a severe fertility defect. Transcriptomic analyis uncovered that PARP-1;PARP-2-deficient mice have defects in the progression of stromal cell decidualization manifesting in pregnancy failure

2021-09-13 | GSE169544 | GEO

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.

2025-01-01 | GSE269408 | GEO

Loss of endometrial plasticity in recurrent pregnancy loss (MeDIP-Seq)

Project description:Decidual transformation of the human endometrium is not dependent on embryo implantation. Instead, this process is initiated during the mid-luteal phase of each cycle in response to the postovulatory rise in progesterone and increasing endometrial cAMP levels. Consequently, decidualization is a reiterative process directly linked to cyclic activation of mesenchymal stem cells (MSCs) and subsequent differentiation into mature stromal cells in regenerating endometrium. We reasoned that aberrant remodeling of the HESC epigenome would disrupt decidualization in RPL patients and account for the functional memory of HESCs in culture. To explore this possibility, we performed MeDIP-seq, which involves immunoprecipitation of DNA with a 5-methylcytosine antibody followed by deep sequencing, on primary HESC cultures established from four RPL patients and four control subjects. Eight samples were analyzed: derived from four control and four recurrent pregnancy loss (RPL) patient cultures.

2015-09-16 | E-GEOD-65100 | biostudies-arrayexpress

Deficiency of PARP-1 and PARP-2 in the mouse uterus results in decidualization failure and pregnancy loss.

Project description:Miscarriage is a common complication of pregnancy for which there are few clinical interventions. Deficiency in endometrial stromal cell decidualization is considered a major contributing factor to pregnancy loss; however, our understanding of the underlying mechanisms of decidual deficiency are incomplete. ADP ribosylation by PARP-1 and PARP-2 has been linked to physiological processes essential to successful pregnancy outcomes. Here, we report that the catalytic inhibition or genetic ablation of PARP-1 and PARP-2 in the uterus lead to pregnancy loss in mice. Notably, the absence of PARP-1 and PARP-2 resulted in increased p53 signaling and an increased population of senescent decidual cells. Molecular and histological analysis revealed that embryo attachment and the removal of the luminal epithelium are not altered in uterine Parp1, Parp2 knockout mice, but subsequent decidualization failure results in pregnancy loss. These findings provide evidence for a previously unknown function of PARP-1 and PARP-2 in mediating decidualization for successful pregnancy establishment.

| S-EPMC8501838 | biostudies-literature

Single-cell sequencing reveals a delicate molecular and cellular interaction during decidualization in humans

Project description:Proper decidualization is a critical determinant of pregnancy success. Deficiencies in decidualization are associated with a variety of pregnancy disorders, including female infertility, recurrent implantation failure, and miscarriage. However, the mechanism for triggering decidualization of human endometrium is largely unknown. Here we characterized the transcriptomes of four major cells in human endometrium and decidua at single-cell resolution. We discovered the dynamic change characteristics of six major stromal cells. More importantly, a dialogue between IGF1+ stromal cells and IGF1R+ stromal cells initiates endometrial decidualization under regulation of progesterone and estrogen, and IL1B+ stromal cells trigger the apoptosis of epithelial cells and functional remodeling during decidualization. We defined a unique AREG+ NK cell for accelerating decidualization by interacting with IGF1+ stromal cells, and observed that extravillous trophoblasts promote decidualization possibly by multiply pathways. Additionally, we developed a systematic repository of cell-cell communication for decidualization via the ligand-receptor complexes interactions. Our study provides deeper insights into the molecular and cellular characterizations during decidualization.

2022-11-24 | GSE194219 | GEO

Tubal ectopic pregnancy as a model to identify endometrial genes and signaling pathways important in decidualization and regulated by local trophoblast

Project description:Gestation-matched endometrium was collected from women with ectopic pregnancy (EP) (n=11) and intrauterine pregnancies (IUP) (n=13). RNA was extracted from the tissue. In addition, tissues were prepared for histological analysis for degree of decidualization. We compared a) the samples from EP that were decidualized (n=6) with non-decidualized samples (n=5), and b) the decidualized EP (n=6) with decidualization-matched IUP (n=6) samples.

2011-07-01 | E-MTAB-680 | biostudies-arrayexpress

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.

2023-10-11 | PXD034357 | Pride

Comparative analysis of mouse decidualization models by using RNA-seq

Project description:There are three well-established mouse models of decidualization: natural pregnancy decidualization (NPD), artificial decidualization (AD) and in vitro decidualization (IVD). In the present study, we analyzed global gene expression changes by using RNA-seq.

2018-11-10 | GSE122376 | GEO

Uterine glands synchronize embryo-endometrial interactions and coordinate on-time embryo implantation and stromal cell decidualization for pregnancy success

Project description:By employing FOXA2-deficient mouse models coupled with LIF repletion, we reveal definitive roles of uterine glands in pregnancy establishment.These studies provide original evidence that uterine glands synchronize embryo-endometrial interactions, coordinate on-time embryo implantation, and impact stromal cell decidualization, thereby ensuring embryo viability, placental growth, and pregnancy success.

2018-04-13 | GSE113065 | GEO

Comparative proteomics analysis of chorionic villi in recurrent pregnancy loss

Project description:The project aimed to determine proteomics changes in chorionic villi from patients suffering from unexplained early recurrent pregnancy loss (RPL) compared to women undergoing elective abortions. Comparative proteomics analysis by label-free data-independent LC-MS/MS was performed on fresh frozen chorionic villi from 13 RPL patients and 10 controls. Samples from EPL patients were preselected to include only patients with 2 or more recurrent pregnancy losses (RPL), no previous live birth, gestational week from 6-10 weeks and excluded fetal chromosomal abnormalities. Control samples were from women without history of previous miscarriage, ectopic pregnancy or preterm delivery, with at least one live born child, at 6-10 gestational weeks and without fetal chromosomal abnormalities. Patients and controls were between 24-44 years with no significant differences among groups regarding age (Median age RPL = 29; Median age Controls = 34; Mann–Whitney U-test p = 0.078). The mean gestational weak (GW) was 7.9±0.8 weeks in the RPL group and 8.3±1.2 weeks in the control group, without statistically significant difference between groups (Median GW RPL = 8; Median GW Controls = 8; Mann–Whitney U-test p = 0.484).

2024-08-27 | PXD048344 | Pride

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