Single-cell Transcriptomics of Endometrial Cells from Patients with Minimal/mild Endometriosis.
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA885152 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21747100_1.fastq.gz | Fastqsanger.gz | |||
| SRR21747100_2.fastq.gz | Fastqsanger.gz | |||
| SRR21747200_1.fastq.gz | Fastqsanger.gz | |||
| SRR21747200_2.fastq.gz | Fastqsanger.gz | |||
| SRR21747101_1.fastq.gz | Fastqsanger.gz |
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Project description:Background: Endometriosis affects approximately 10% of reproductive age women and 30%-50% of infertile women. Decreased endometrial receptivity is mainly responsible for infertile women with minimal/mild endometriosis. Medical therapy to improve fecundity of these women is needed. Metformin is reported to inhibit growth of ectopic lesions in endometriosis, while the effect on eutopic endometrium is unclear. The study was to identify if metformin had effect on eutopic endometrium in women with minimal/mild endometriosis and thus improve their fecundity. Materials and Methods: Paired endometrial tissues of secretory phase from participants with minimal/mild endometriosis were collected before and after two months of metformin treatment and setting metformin-free control. Protein expression profiles of endometrium were analyzed by proteomics. Results: A total of 115 proteins were detected up-regulated after metformin therapy, including Insulin-like growth factor-binding protein 7, α-antitrypsin, apolipoprotein D, Rho GDP-dissociation inhibitor 1, brain form glycogen phosphorylase, and Cathepsin B that associated with endometrial receptivity, while there had no significant changes in controls. These up-regulated markers were validated through target proteomics and further demonstrated with endometriosis mice models. Conclusions: This study revealed that metformin might ameliorate biomarkers expressions of endometrial receptivity in human and mice model. Metformin is potential to improve endometrial receptivity of endometriosis-associated infertility.
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Project description:Alterations in endometrial DNA methylation profile have been proposed as one potential mechanism initiating the development of endometriosis. However, the normal endometrial methylome is influenced by the cyclic hormonal changes and the menstrual cycle phase-dependent epigenetic signature should be considered when studying endometrial disorders. So far, no studies have been performed to evaluate the menstrual cycle influences and endometriosis-specific endometrial methylation pattern at the same time. Therefore, we used Infinium HumanMethylation 450K BeadChip arrays to explore DNA methylation profiles of endometrial tissues from various menstrual cycle phases.
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