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Hypoxia-inducible factor 1 signaling drives placental aging and can elicit inflammatory changes in uterine myocytes

ABSTRACT: Hypoxia-inducible factor 1 signaling drives placental aging and can elicit inflammatory changes in uterine myocytes

PROVIDER: PRJNA819113 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18458333_1.fastq.gz	Fastqsanger.gz
	SRR18458333_2.fastq.gz	Fastqsanger.gz
	SRR18458334_1.fastq.gz	Fastqsanger.gz
	SRR18458334_2.fastq.gz	Fastqsanger.gz
	SRR18458335_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Hypoxia-inducible factor 1 signaling drives placental aging and can elicit inflammatory changes in uterine myocytes

Project description:Placental aging has been proposed to promote labor onset, but specific mechanisms remain elusive. An unbiased transcriptomic analysis of healthy mouse placenta revealed that hypoxia-inducible factor 1 (HIF-1) stabilization is a hallmark of advanced gestational timepoints, accompanied by mitochondrial dysfunction and cellular senescence. We validated these gestational age-associated changes through similar findings in human placenta. In parallel in primary mouse trophoblasts and human choriocarcinoma JAR cells, we modeled HIF-1 induction using prolyl hydroxylase inhibitors cobalt chloride (CoCl2) and dimethyloxalylglycine (DMOG), and demonstrated that mitochondrial dysfunction and cellular senescence occur secondary to HIF-1 stabilization. Whole transcriptome analysis revealed that HIF-1 stabilization in JAR cells recapitulated the dysregulation of several pathways observed in aged placenta. Further, conditioned media from cultured trophoblasts following HIF-1 induction is sufficient to induce a contractile phenotype in immortalized uterine myocytes, suggesting a mechanism by which the aging placenta may help drive the transition from uterine quiescence to contractility at the onset of labor.

2022-03-29 | GSE199278 | GEO

Conservation at the uterine-placental interface

Project description:Conservation at the uterine-placental interface

| PRJNA849158 | ENA

Conservation at the uterine-placental interface

Project description:The hemochorial placentation site is characterized by a dynamic interplay between trophoblast cells and maternal cells. These cells cooperate to establish an interface required for nutrient delivery to promote fetal growth. In the human, trophoblast cells penetrate deep into the uterus. This is not a consistent feature of hemochorial placentation and has hindered the establishment of suitable animal models. The rat represents an intriguing model for investigating hemochorial placentation with deep trophoblast cell invasion. In this study, we used single cell RNA sequencing to characterize the transcriptome of the invasive trophoblast cell lineage, as well as other cell populations within the rat uterine-placental interface during early (gestation day, gd, 15.5) and late (gd 19.5) stages of intrauterine trophoblast cell invasion. We identified a robust set of transcripts that define invasive trophoblast cells, as well as transcripts that distinguished endothelial, smooth muscle, natural killer, and macrophage cells. Invasive trophoblast, immune, and endothelial cell populations exhibited distinct spatial relationships within the uterine-placental interface. Furthermore, the maturation stage of invasive trophoblast cell development could be determined by assessing gestation-stage dependent changes in transcript expression. Finally, and most importantly, expression of a prominent subset of rat invasive trophoblast cell transcripts is conserved in the invasive extravillous trophoblast cell lineage of the human placenta. These findings provide foundational data to identify and interrogate key conserved regulatory mechanisms essential for development and function of an important compartment within the hemochorial placentation site that is essential for a healthy pregnancy.

2022-09-20 | GSE206086 | GEO

Placental growth factor mediates pathological uterine vasculature by activating the NFAT5-SGK1 mechano-signaling axis in the endometrium: Implications for pre-eclampsia development.

Project description:After menstruation the uterine spiral arteries are repaired through angiogenesis. This process is tightly regulated by the paracrine communication between endometrial stromal cells (EnSCs) and endothelial cells. Any molecular aberration in these processes can lead to complications in pregnancy including miscarriage or pre-eclampsia (PE). Placental growth factor (PlGF) can increase cell stiffness contributing to pathological angiogenesis but the biomechanisms remain poorly understood. In this study, we investigated whether PlGF contributes to pathological uterine vasculature by disrupting EnSCs and endothelial paracrine communication. We observed that PlGF mediates a tonicity-independent activation of nuclear factor of activated T cells 5 (NFAT5) in EnSCs. NFAT5 activated downstream targets including SGK1, HIF-1α and VEGF-A. In depth characterization of PlGF - conditioned medium (CM) from EnSCs using mass spectrometry and ELISA methods revealed low VEGF-A and an abundance of extracellular matrix organization associated proteins. Secreted factors in PlGF-CM impeded normal angiogenic cues in endothelial cells (HUVECs) by downregulating Notch-VEGF signalling. Interestingly, PlGF-CM failed to support human placental (BeWo) cell invasion through HUVEC monolayer. Inhibition of SGK1 in EnSCs improved angiogenic effects in HUVECs and promoted BeWo invasion, revealing SGK1 as a key intermediate player modulating PlGF mediated anti-angiogenic signalling. Taken together, perturbed PlGF-NFAT5-SGK1 mechano-signaling in the endometrium can contribute to pathological uterine angiogenesis by negatively regulating EnSCs -endothelial crosstalk resulting in poor quality vessels in the uterine microenvironment. Taken together the signaling may impact on normal trophoblast invasion and thus placentation and, may be associated with an increased risk of complications such as PE.

2024-10-17 | PXD051697 | Pride

Placental ischemia induces changes in gene expression in chorionic tissue

Project description:Microarray analysis of differentially expressed genes from rats undergoing placental ischemia versus health controls Placental ischemia is believed to be an important contributor to human preeclampsia, though the targets induced by the ischemia remain unclear. Chorionic placental tissues from 6 control and 6 placental ischemic reduced uterine perfusion pressure (RUPP) rats were analyzed for gene expression by microarray.

2013-09-05 | E-GEOD-50596 | biostudies-arrayexpress

Increased apoptosis, altered oxygen signalling and antioxidant defenses in first trimester pregnancies with high resistance uterine artery blood flow

Project description:High uterine artery Doppler (UtAD) resistance indices (RI), indicative of poor uterine blood flow, have been shown to be predictive of placental complications of pregnancy such as pre-eclampsia (PE), fetal growth restriction (FGR) and stillbirth. A comparative analysis of gene expression in High vs normal risk pregnancies in placental tissue from first trimester was undertaken. Patients were stratified by their risk of developing placental complications as determined by Doppler resistance indices. High-resistance cases were defined as those with bilateral uterine diastolic notches and a mean RI >95th percentile whilst Normal-resistance cases had a mean RI of <95th percentile. A direct comparison of gene expression in Placental villous tissue obtained folowing terminations at of 9 to 14 weeks gestation.

2015-07-22 | E-MTAB-3265 | biostudies-arrayexpress

Liquid crystal monomers induce placental development and progesterone release dysregulation through transplacental transportation

Project description:Embryonic and fetal development can be affected during gestation by exposure to xenobiotics that cross the placenta. Liquid crystal monomers (LCMs) are emerging contaminants commonly found in indoor environments; however, whether they can cross the placenta and affect placental development remains unexplored. Here, we developed an evaluation system that integrates human biomonitoring, uterine perfusion in pregnant rats, and placental cells. We found fourteen out of the fifty-six LCMs that were detected in maternal and cord serum samples from ninety-three healthy pregnant women, at median levels of 13.9 and 18.1 ng/mL, respectively. Subsequent exploration of in utero exposure in rats indicated that aromatic amino acid transporter 1 (SLC16A10) mediated transplacental transportation of the LCMs. Placental cells exposed to LCMs exhibited delayed placental development and reduced progesterone release. These findings showed that SLC16A10-mediated transplacental transportation of LCMs inhibits placental development and progesterone release, highlighting the importance of gestational exposure to emerging contaminants.

2025-01-21 | PXD059395 | Pride

Prenatally androgenized PCOS mice have ovary-independent uterine dysfunction and placental inflammation aggravated by high-fat diet

Project description:Polycystic ovary syndrome (PCOS) is a common hyperandrogenic and metabolic condition in women. The syndrome is linked to subfertility and pregnancy complications, yet the independent effects of exposure to hyperandrogenism and obesity on endometrial function remain unclear. Here, PCOS-like mice were generated using prenatal androgenization (PNA) with dihydrotestosterone, followed by a prepubertal high-fat (HF) or standard diet. In ovariectomized mice, PNA impaired uterine closure during the implantation window, disrupted decidualization, and altered extracellular matrix- and inflammation-related gene expression. The effects were aggravated by HF diet. In naturally mated, ovary-intact mice, PNA and HF diet affected decidual and placental gene expression, suggestive of placental dysfunction and inflammation, and induced fetal growth restriction. This study underlines the role of the uterus in adverse pregnancy outcomes in PCOS and identifies possible underlying mechanisms for future studies. Pre-pregnancy interventions targeting metabolic health and hyperandrogenism should be the next steps to optimize PCOS pregnancy outcomes.

2025-04-10 | GSE278408 | GEO

Uterine Influences on Conceptus Development in Fertility-Classified Animals

Project description:This study relates to pregnancy outcome after assisted reproduction of fertility-classified cattle. The aim is to investigate how the uterine environment impacts and programs conceptus survival and development. The study found that ripple effects of dysregulated conceptus-endometrial interactions elicit post-elongation pregnancy loss in subfertile animals during the implantation period.

2017-12-12 | GSE107891 | 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

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