Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6920380_1.fastq.gz | Fastqsanger.gz | |||
| SRR6920380_2.fastq.gz | Fastqsanger.gz | |||
| SRR6920390_1.fastq.gz | Fastqsanger.gz | |||
| SRR6920390_2.fastq.gz | Fastqsanger.gz | |||
| SRR6920400_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 136 |
Similar Datasets
Project description:The transgenerational maternal effects of PCOS in female progeny have been revealed. As there are evidence that a male equivalent of PCOS may exist, we asked whether sons born to mother with PCOS (PCOS-sons) transmit reproductive and metabolic phenotypes to their male progeny. Here, in a Swedish nationwide register-based cohort and a clinical case-control study from Chile we found that PCOS-sons are more often obese and dyslipidemic. Their serum miRNAs are found to potentially regulate PCOS-risk genes. Our prenatal androgenized PCOS-like mouse model with or without diet-induced obesity confirmed that reproductive and metabolic dysfunctions in F1 male offspring are passed down to F3. Small non-coding RNAs (sncRNAs) sequencing of F1-F3 sperm revealed distinct differentially expressed (DE) sncRNAs across generations in the androgenized, obese, and obese and androgenized lineages, respectively. Notably, common targets between transgenerational DEsncRNAs in mouse sperm and in PCOS-sons serum indicate similar effects of maternal hyperandrogenism. These findings strengthen the translational relevance highlighting a previously underappreciated risk of reproductive and metabolic dysfunction via the male germline transmission and potential molecular markers to study in future generations.
| EGAS00001007079 | EGA
Project description:<p><strong>BACKGROUND:</strong> Polycystic ovarian syndrome (PCOS) is a common endocrine disorder characterized by hyperandrogenism, ovarian dysfunction and polycystic ovarian morphology. Gut microbiota dysbiosis and metabolite are associated with PCOS clinical parameters. Yulin Tong Bu formula (YLTB), a traditional Chinese medicine formula, has been recently indicated to be capable of ameliorating polycystic ovary symptoms and correcting abnormal glucose metabolism. However, the therapeutic mechanism of YLTB on PCOS has not been fully elucidated.</p><p><strong>METHODS:</strong> A pseudo sterile mouse model was established during this 4-day acclimatization phase by giving the animals an antibiotic cocktail to remove the gut microbiota. Here, the therapeutic effects of YLTB on PCOS were investigated using dehydroepiandrosterone plus high-fat diet induced PCOS mice model. Female prepuberal mice were randomly divided into 3 groups; namely, the control group, PCOS group and YLTB (38.68 g/kg/day) group. To test whether this effect is associated with the gut microbiota, we performed 16S rRNA sequencing studies to analyze the fecal microbiota of mice. The relationships among metabolites, gut microbiota and PCOS phenotypes were further explored by using Spearman correlation analysis. Then, the effect of metabolite ferulic acid was then validated in PCOS mice.</p><p><strong>RESULTS:</strong> Our results showed that YLTB treatment ameliorated PCOS features (ovarian dysfunction, delayed glucose clearance, decreased insulin sensitivity, deregulation of glucolipid metabolism and hormones, etc) and significantly attenuated PCOS gut microbiota dysbiosis. Spearman correlation analysis showed that metabolites such as ferulic acid and folic acid are negatively correlated with PCOS clinical parameters. The effect of ferulic acid was similar to that of YLTB. In addition, the bacterial species such as <em>Bacteroides dorei</em> and <em>Bacteroides fragilis</em> were found to be positively related to PCOS clinical parameters, using the association study analysis.</p><p><strong>CONCLUSION:</strong> These results suggest that YLTB treatment systematically regulates the interaction between the gut microbiota and the associated metabolites to ameliorate PCOS, providing a solid theoretical basis for further validation of YLTB effect on human PCOS trials.</p>
2023-02-02 | MTBLS6736 | MetaboLights
Project description:Polycystic ovary syndrome (PCOS) is a heterogeneous endocrine disorder characterized by hyperandrogenism, ovulatory dysfunction, and polycystic ovaries. In this study, we induced a PCOS rat model by oral administration of letrozole combined with a high-fat diet and then treated with mogroside V (MV) to evaluate the protective roles on endocrine and follicle development in PCOS rats and the underlying mechanisms. Purpose: To detect the difference of ovary transcriptome profiling between PCOS model and Control rat and to evaluate the effect of mogroside V on the transcriptome profiling of ovaries of PCOS model rats. Methods: Ovarian mRNA profiles of 15-week-old Control, PCOS and PCOS-MV group rats (4 rats per group) were generated by deep sequencing,using Illumina PE150.
2022-04-20 | GSE194398 | GEO
Project description:To investigate the etiology of the hyperandrogenic phenotype of polycystic ovary syndrome (PCOS), a prenatally androgenized (PNA) mouse model was validated and used for microarray analysis.
2017-11-01 | GSE103056 | GEO
Project description:Genome-wide association studies (GWAS) have identified polycystic ovary syndrome (PCOS)-associated loci, including DENND1A encoding a clathrin-binding protein involved in vesicle transport as a guanine nucleotide exchange factor. The effect of DENND1A on reproduction and whether it participates in follicle development disorder and androgen synthesis in PCOS remain unknown. Here, we demonstrated that DENND1A expression increased in ovarian granulosa cells (GCs) of PCOS patients and was positively correlated with serum testosterone concentration. We constructed a systemic transgenic Dennd1a mouse (TG mouse) model, which showed subfertility, irregular estrous cycles, and increased production of testosterone after PMSG stimulation. Moreover, TG mice showed hyporesponsiveness to PMSG with smaller ovary size and less well-developed follicles. Intracellular follicle-stimulating hormone receptor (FSHR) transport was disturbed by overexpression of Dennd1a, which promoted FSHR internalization and inhibited its recycling. Our findings revealed the reproductive function of DENND1A and the underlying mechanisms, which provided new insights into the PCOS pathogenesis and contributing to drug design for PCOS treatment.
2023-07-05 | GSE236248 | GEO
Project description:DNA methylation analysis of oocytes in a PCOS mouse model
| PRJDB12821 | ENA
Project description:In summary, we characterized the role of m6A modification in pulmonary fibrosis. We reveal that m6A modification is increased in bleomycin induced pulmonary fibrosis mice model, FMT-derived myofibroblasts and idiopathic pulmonary fibrosis patient lung samples. Lowering m6A level through silencing METTL3 suppress FMT process in vitro and vivo. Fundamentally, m6A modification regulates FMT by modulating the translation of KCNH6 mRNA in a YTHDF1 dependent manner. This study provides novel insights into the mechanism of FMT process and suggests m6A modification intervention may be a promising therapeutic strategy for pulmonary fibrosis.
2021-06-02 | GSE164151 | GEO
Project description:To identify a role for protein palmitoylation in ovarian of DHEA-induced PCOS mice model. First, we used DHEA to induce a PCOS mice model，hematoxylin-eosin (H&E) staining sections form the ovaries of the Control and DHEA groups.The mice oral gavage with DHEA disrupted ovarian morphology,the estrous cycle, and hormone profilein DHEA-induced mouse. The three pairs of ovary for each tube are mixed together as a group were lysed and divided into 2 fractions. The -HAM condition served as a negative control and the +HAM sample positive control.In the +HAM sample, the palmitate residue was cleaved off and exchanged with biotin. After the ABE reaction was completed, streptavidin beads were used to enrich for biotinylated proteins. Proteins enriched from +HAM and −HAM conditions were identified using mass spectrometry (MS).
2023-03-11 | PXD028835 | Pride
Project description:Necrotizing enterocolitis (NEC) is an acute and life-threatening gastrointestinal disorder afflicting preterm infants, which is currently unpreventable. Fecal microbiota transplantation (FMT) is a promising preventative therapy, but potential bacterial infection raise concern. Removal of bacteria from donor feces may reduce this risk while maintaining the NEC-preventive effects. We aimed to assess preclinical efficacy and safety of bacteria-free fecal filtrate transfer (FFT). Using fecal material from healthy suckling piglets, we administered FMT rectally, or cognate FFT either rectally or oro-gastrically to formula-fed preterm, cesarean-delivered piglets as a model for preterm infants, We compared gut pathology and related safety parameters with saline controls, and analyzed ileal mucosal transcriptome to gauge the host e response to FMT and FFT treatments relative to control. Results showed that oro-gastric FFT prevented NEC, whereas FMT did not perform better than control. Moreover, FFT but not FMT reduced intestinal permeability, whereas FMT animals had reduced body weight increase and intestinal growth. Global gene expression of host mucosa responded to FMT but not FFT with increased and decreased bacterial and viral defense mechanisms, respectively. In conclusion, as preterm infants are extremely vulnerable to enteric bacterial infections, rational NEC-preventive strategies need incontestable safety profiles. Here we show in a clinically relevant animal model that FFT, as opposed to FMT, efficiently prevents NEC without any recognizable side effects. If translatable to preterm infants, this could lead to a change of practice and in turn a reduction in NEC burden.
2021-10-01 | GSE158878 | GEO