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ABSTRACT: transcriptome sequencing of unexplained recurrent spontaneous abortion

PROVIDER: PRJNA771930 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16370906_1.fastq.gz	Fastqsanger.gz
	SRR16370906_2.fastq.gz	Fastqsanger.gz
	SRR16370907_1.fastq.gz	Fastqsanger.gz
	SRR16370907_2.fastq.gz	Fastqsanger.gz
	SRR16370908_1.fastq.gz	Fastqsanger.gz

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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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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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