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ABSTRACT: Transcriptome sequencing of decidua in patients with unexplained recurrent spontaneous abortion

PROVIDER: PRJNA819201 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18458956_1.fastq.gz	Fastqsanger.gz
	SRR18458956_2.fastq.gz	Fastqsanger.gz
	SRR18458957_1.fastq.gz	Fastqsanger.gz
	SRR18458957_2.fastq.gz	Fastqsanger.gz
	SRR18458958_1.fastq.gz	Fastqsanger.gz

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Epigenome analysis of decidua tissues from unexplained recurrent spontaneous abortion patients and controls with induced abortions

Project description:Genome wide DNA methylation profiling of decidua samples from unexplained recurrent spontaneous abortion patients and controls with induced abortions. The Infinium Human Methylation 850K BeadChip was used to obtain DNA methylation profiles across approximately 853,307 CpGs in decidua samples . Samples included 2 normal pregnant women (non-medical reasons for abortion) and 4 unexplained recurrent spontaneous abortion patients.

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Single cell transcriptome analysis of decidua macrophages in normal and recurrent spontaneous abortion patients

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Characteristic DNA methylation profiles of chorionic villi in recurrent miscarriage

Project description:Genome wide DNA methylation profiling of chorionic villi and decidua from recurrent miscarriage patients and artificial abortion controls. Infinium HumanMethylation450 BeadChip was used.

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The transcription factor PBX1 drives natural killer cells to promote fetal development

Project description:Perfect fetal development is a solid foundation for successful fertility, in which the abundant natural killer (NK) cells in the decidua tissue at the maternal-fetal interface play an important role during the first trimester. The functional subsets and transcriptional regulation mechanisms of decidual NK (dNK) cells remain poorly understood. Here, we identified CD49a+PBX1+ dNK cells as a unique subset of NK cells that promote fetal development in both human and mice. PBX1 drove the transcription of key functional molecules pleiotrophin and osteoglycin that promote fetal development through direct promoter binding. In patients with unexplained recurrent spontaneous abortion (URSA), decreased expression of PBX1 and PBX1(G21S) mutation correlated with fetal growth restriction and pregnancy failure. Inactivation of Pbx1 in mouse NK cells caused impaired fetal development due to a decrease in growth promoting factors. Our observations reveal the molecular regulation mechanism of CD49a+PBX1+ dNK cells promoting fetal development, and indicate that impaired PBX1 in dNK cells may serve as pathogenesis and biomarker of URSA.

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Mouse placenta in spontaneous abortion

Project description:Genetic profiles of mouse placenta were examined especially at the implantation sites of causing spontaneous abortion at day 14.5 of pregnancy. There is a number of the suffered patients from the recurrent spontaneous abortion by unknown causes. It is an important process to understand genetic profiles in the abortion placentas for the investigation of specific causes to induce rejection of normal embryos from the maternal attack. Our study was carried out on the laboratory mice targeted spontaneous abortion to approximate human disease models.

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Single-cell sequencing and second-generation RNA sequencing-based screening of macrophage-associated marker genes for recurrent miscarriage diagnosis

Project description:We profiled the transcriptomes of about 110000 single cells from 16 human first-trimester decidual and villi samples from 5 normal samples and 3 recurrent miscarriage (RM) samples. Each decidual and villi samples was collected from the same patient. The cellular composition revealed five major subsets of immune cells including NK, T cell, macrophage, monocytes and B cell in the maternal fetal interface. We used the marker gene of macrophages to establish the diagnosis and treatment model of unexplained recurrent abortion, in order to explore the relationship between immune cells and unexplained recurrent abortion.

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