Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptome analyses of trophoblast upon hypoxia or normoxia

ABSTRACT: The hypoxia inducible molecules are proposed to be one of many key regulators of first trimester trophoblast behavior, but the key mechanism mediating invasion of trophoblast cells is not very clear.

ORGANISM(S): Homo sapiens

PROVIDER: GSE128114 | GEO | 2024/03/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

m1A-Seq analyses of trophoblast upon hypoxia or normoxia

Project description:N1-methyladenosine (m1A) is one of messenger RNA modification in eukaryotes, but the potential roles of m1A methylated mRNA in trophoblast upon hypoxia remain elusive.

2020-03-24 | GSE135403 | GEO

m6A-Seq analyses of trophoblast upon hypoxia or normoxia

Project description:N6-methyladenosine (m6A) is the most prevalent messenger RNA modification in eukaryotes, but the potential roles of m6A methylated mRNA in trophoblast upon hypoxia remain elusive.

2024-03-01 | GSE128116 | GEO

m1A-Seq analyses of trophoblast upon hypoxia or normoxia

Project description:m1A-Seq analyses of trophoblast upon hypoxia or normoxia

| PRJNA558765 | ENA

Hypoxia induced HIF-1/HIF-2 activity alters trophoblast transcriptional regulation and promotes invasion

Project description:Reduced or absent cytotrophoblast invasion of the maternal uterine spiral arteries is a common clinical finding in studies of pregnancies complicated by preeclampsia, suggesting that the mechanisms behind invasion of these cells is perturbed. The placenta initially develops in a low oxygen environment of 1-2% oxygen until after the 10th week of pregnancy. During this time oxygen concentration exerts a major influence over trophoblast activity and, in vitro, hypoxia inducible factors are proposed to be one of many key regulators of first trimester trophoblast behaviour. We used a global gene expression microarray approach to identify signalling pathways involved in invasion of the first trimester trophoblast cell line HTR8/SVneo under hypoxic conditions where HIF-1 was active. Additionally, first trimester placental samples from different gestational age groups were labelled with anti HIF-1 and HIF-2 to evaluate whether HIFs are differentially expressed and localised across the period of development characterised by hypoxia (6-8 weeks) and maternal blood perfusion (10-12 weeks). Eighty-eight genes were differentially expressed between cells cultured in 1% oxygen (where HIF-1 was localised to the nucleus) and 5% oxygen (where HIF-1 was cytoplasmic). 65% of the genes were predicted to contain HIF-1α:ARNT transcription factor binding sites. Increased nuclear localisation of HIF-1α was seen in extravillous cytotrophoblasts in early first trimester compared with late, while cellular expression of HIF-2α in the villous stroma was higher in late first trimester. While HIFs and their downstream targets are clearly induced in trophoblasts during early placental development, and in vitro hypoxic conditions, the mechanism and pathways by which invasion is increased under hypoxic conditions is not clear from the gene expression profile. Further insight beyond the transcription level is required to fully understand this complex phenomenon.

2015-10-01 | GSE65271 | GEO

EP001: The interferon transcriptome in uterine NK cells is upregulated during the second trimester of pregnancy allowing extravillous trophoblast invasion

Project description:Uterine Natural Killer (uNK) cells regulate essential developmental processes at the maternal-fetal interface during early pregnancy. Uterine NK cell functions are tightly regulated during early placentation to stimulate trophoblast invasion and remodel uterine spiral arteries. Access to human 1st and 2nd trimester uterine tissues allowed us to investigate the transcriptional changes in uNK cells during the early stages of early human pregnancy. Microarray analysis identified 97 upregulated genes in 2nd compared to 1st trimester purified uNK cells of which the majority (61%) clustered as interferon-stimulated-genes (ISG), with ISG15 and ISG20 being upregulated profoundly. Type I interferons (IFNα/β), but not type II interferon (IFNɣ) increased expression of the identified interferon target genes ISG15 and ISG20 in uNK cells in vitro. Moreover, the cytokine-like protein ISG15 stimulated in vitro trophoblast invasion. Second trimester uNK cells promoted trophoblast invasion in vitro, whereas both 1st and 2nd trimester uNK cells stimulated endothelial tube formation. IFNα but not IFNβ stimulation of 1st trimester uNK cells enhanced their capacity to promote trophoblast invasion. In conclusion, the uNK cell interferon transcriptome is upregulated during the 2nd trimester allowing uNK cells to promote trophoblast invasion. Type I interferon signaling regulates uNK cell-induced trophoblast invasion via induction of effector molecules like ISG15. First trimester uNK cells can be induced to act like second trimester uNK cells by IFNα with respect to promotion of trophoblast invasion. Key words: Gene expression profiling ■ uterine natural killer cells ■ extravillous trophoblast invasion ■ interferon alpha ■ ISG15

2020-01-30 | GSE64898 | GEO

Transcriptome analyses of trophoblast upon YTHDF3 knockdown

Project description:YTHDF3 play important role in regulation of trophoblast activity, we examined the downstream genes of YTHDF3 via transcriptome sequencing

2020-03-24 | GSE135407 | GEO

Transcriptome analyses of trophoblast upon ALKBH5 knockdown

Project description:ALKBH5 play important role in regulation of trophoblast invasion, we examined the downstream genes of ALKBH5 via transcriptome sequencing

2019-03-12 | GSE128096 | GEO

Hypoxia induces trophoblast migration and invasion gene pathways, a subset of which are reduced in preeclampsia

Project description:Placentation requires the proper regulation of extravillous trophoblast (EVT) migration and invasion into the decidua and maternal vasculature, processes which are initiated in physiologic hypoxic conditions. Abnormal EVT migration and/or invasion have been suggested to lead to pregnancy complications, such as preeclampsia. The objectives of this study are to determine how exposure to hypoxia impacts gene expression and cellular motility of first trimester trophoblasts, and to assess if expression of migration-associated genes is dysregulated in 2nd trimester chorionic villous samples (CVS) from preeclampsia pregnancies relative to CVS from healthy pregnancies. The 1st trimester trophoblast cell line, HTR8/SVneo, was used to investigate the relationship between hypoxia and Notch signaling in trophoblast migration and invasion. RNA sequencing and quantitative RT-PCR analyses show that exposure to hypoxia (2.5% O2) activates Notch signaling in HTR-8/SVneo. We demonstrate that exposure of HTR-8/SVneo to hypoxia induces expression of genes associated with cellular migration and invasion and increases HTR-8/SVneo cellular migration and invasion, whereas inhibition of gamma-secretase decreases Notch signaling and decreases HTR-8/SVneo migration and invasion. Analysis of RNA sequencing data from CVS of preeclampsia and uncomplicated pregnancies identified significant differentially expressed genes that are involved in cellular migration and invasion. Decreased expression of migration and invasion genes in CVS from preeclampsia pregnancies, may impair trophoblast migration and invasion in the 2nd trimester of pregnancy, resulting in the development of preeclampsia.

2021-08-05 | GSE155750 | GEO

Transcriptome analyses of trophoblast upon ALKBH5 knockdown

Project description:Transcriptome analyses of trophoblast upon ALKBH5 knockdown

| PRJNA526448 | ENA

Transcriptome analyses of trophoblast upon YTHDF3 knockdown

Project description:Transcriptome analyses of trophoblast upon YTHDF3 knockdown

| PRJNA558768 | ENA