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Impaired bone morphogenetic protein signaling pathways perturb decidualization in patients with endometriosis (Cut&Run-Seq)

ABSTRACT: Impaired bone morphogenetic protein signaling pathways perturb decidualization in patients with endometriosis (Cut&Run-Seq)

PROVIDER: PRJNA1016445 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26056941_1.fastq.gz	Fastqsanger.gz
	SRR26056941_2.fastq.gz	Fastqsanger.gz
	SRR26056942_1.fastq.gz	Fastqsanger.gz
	SRR26056942_2.fastq.gz	Fastqsanger.gz
	SRR26056943_1.fastq.gz	Fastqsanger.gz

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Impaired bone morphogenetic protein signaling pathways perturb decidualization in patients with endometriosis

Project description:Impaired bone morphogenetic protein signaling pathways perturb decidualization in patients with endometriosis

| PRJNA1016440 | ENA

Impaired bone morphogenetic protein signaling pathways perturb decidualization in patients with endometriosis (Cut&Run-Seq)

Project description:It is hypothesized that impaired endometrial decidualization contributes to decreased fertility in endometriosis patients. To identify the molecular defects that underpin defective decidualization in endometriosis, we subjected endometrial stromal cells from healthy individuals or with endometriosis to time course in vitro decidualization with estradiol, progesterone, and 8-bromo-cyclic-AMP (EPC) for 2, 4, 6, or 8 days. Transcriptomic profiling identified novel differences in key pathways between normal and endometriosis, including defective bone morphogenetic protein (BMP) signaling (ID1, ID2, ID3, BMP6), altered iron transport (SLC40A1, TFRC), endometrial stem cell markers (CD44, SUSD2), and retinoid signaling pathways (RORB, ALDH1L1, RARA). Genome-wide binding analyses identified an altered genomic distribution of SMAD4 in decidualized stromal cells from endometriosis patients relative to normal individuals, with an overrepresentation of gene ontologies related to signaling by transforming growth factor β (TGFβ), neurotrophic tyrosine kinase receptors (NTRK), and nerve growth factor (NGF)-stimulated transcription. We found that direct SMAD1/5/4 target genes control FOXO, PI3K/AKT, and progesterone-mediated signaling in decidualizing cells and that BMP2 supplementation of patient-derived assembloids from endometriosis patients restored decidualization. In summary, transcriptomic and genomic profiling of patient-derived endometrial cells and assembloids identified that restoring BMP/SMAD1/5/4 signaling is crucial for engaging a robust decidualization program in women with endometriosis.

2024-02-17 | GSE243156 | GEO

Impaired bone morphogenetic protein signaling pathways perturb decidualization in patients with endometriosis (SMAD1/5 siRNA studies)

2024-02-17 | GSE243157 | GEO

Impaired bone morphogenetic protein signaling pathways perturb decidualization in patients with endometriosis (Time-course EPC studies)

2024-02-17 | GSE243039 | GEO

Impaired bone morphogenetic protein signaling pathways perturb decidualization in patients with endometriosis (Time-course EPC studies)

Project description:Impaired bone morphogenetic protein signaling pathways perturb decidualization in patients with endometriosis (Time-course EPC studies)

| PRJNA1016267 | ENA

Impaired bone morphogenetic protein signaling pathways perturb decidualization in patients with endometriosis (SMAD1/5 siRNA studies)

Project description:Impaired bone morphogenetic protein signaling pathways perturb decidualization in patients with endometriosis (SMAD1/5 siRNA studies)

| PRJNA1016448 | ENA

Impaired bone morphogenetic protein signaling pathways perturb decidualization in patients with endometriosis

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-02-17 | GSE243158 | GEO

Impaired bone morphogenetic protein signaling pathways disrupt decidualization in endometriosis.

Project description:It is hypothesized that impaired endometrial decidualization contributes to decreased fertility in individuals with endometriosis. To identify the molecular defects that underpin defective decidualization in endometriosis, we subjected endometrial stromal cells from individuals with or without endometriosis to time course in vitro decidualization with estradiol, progesterone, and 8-bromo-cyclic-AMP (EPC) for 2, 4, 6, or 8 days. Transcriptomic profiling identified differences in key pathways between the two groups, including defective bone morphogenetic protein (BMP)/SMAD4 signaling (ID2, ID3, FST), oxidate stress response (NFE2L2, ALOX15, SLC40A1), and retinoic acid signaling pathways (RARRES, RARB, ALDH1B1). Genome-wide binding analyses identified an altered genomic distribution of SMAD4 and H3K27Ac in the decidualized stromal cells from individuals without endometriosis relative to those with endometriosis, with target genes enriched in pathways related to signaling by transforming growth factor β (TGFβ), neurotrophic tyrosine kinase receptors (NTRK), and nerve growth factor (NGF)-stimulated transcription. We found that direct SMAD1/5/4 target genes control FOXO, PI3K/AKT, and progesterone-mediated signaling in decidualizing cells and that BMP2 supplementation in endometriosis patient-derived assembloids elevated the expression of decidualization markers. In summary, transcriptomic and genome-wide binding analyses of patient-derived endometrial cells and assembloids identified that a functional BMP/SMAD1/5/4 signaling program is crucial for engaging decidualization.

| S-EPMC10542516 | biostudies-literature

Impaired bone morphogenetic protein (BMP) signaling pathways disrupt decidualization in endometriosis.

Project description:Endometriosis is linked to increased infertility and pregnancy complications due to defective endometrial decidualization. We hypothesized that identification of altered signaling pathways during decidualization could identify the underlying cause of infertility and pregnancy complications. Our study reveals that transforming growth factor β (TGFβ) pathways are impaired in the endometrium of individuals with endometriosis, leading to defective decidualization. Through detailed transcriptomic analyses, we discovered abnormalities in TGFβ signaling pathways and key regulators, such as SMAD4, in the endometrium of affected individuals. We also observed compromised activity of bone morphogenetic proteins (BMP), a subset of the TGFβ family, that control endometrial receptivity. Using 3-dimensional models of endometrial stromal and epithelial assembloids, we showed that exogenous BMP2 improved decidual marker expression in individuals with endometriosis. Our findings unveil a previously unidentified dysfunction in BMP/SMAD signaling in the endometrium of individuals with endometriosis, explaining decidualization defects and subsequent pregnancy complications in these individuals.

| S-EPMC10659538 | biostudies-literature

Seminal plasma promotes decidualization of endometrial stromal fibroblasts from women with and without inflammatory disorders in a manner dependent on IL11 signaling

Project description:SP promotes decidualization of eSF from women with and without inflammatory disorders (polycystic ovarian syndrome (PCOS), endometriosis) in a manner that is not mediated through semen amyloids and that is associated with a potent transcriptional response including induction of IL11, a cytokine important for SP-induced decidualization.

2020-03-09 | GSE135640 | GEO

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