A high protein model alters the endometrial transcriptome of mares
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA545051 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9133800_1.fastq.gz | Fastqsanger.gz | |||
| SRR9133800_2.fastq.gz | Fastqsanger.gz | |||
| SRR9133801_1.fastq.gz | Fastqsanger.gz | |||
| SRR9133801_2.fastq.gz | Fastqsanger.gz | |||
| SRR9133802_1.fastq.gz | Fastqsanger.gz |
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Project description:We developed an experimental model to elevate BUN during diestrus. There were both urea and control treatments (7 mares/treatment), done in a crossover design. Urea treatment consisted of a loading dose of urea (0.03 g/kg of urea) and urea injections over 6 hours (0.03 g/kg/hr). Control mares received the same volume of saline solution. Blood samples were collected to measure BUN. Uterine and vaginal pH were evaluated after the last intravenous infusion, then endometrial biopsies were collected for RNA-sequencing
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Project description:High blood urea nitrogen (BUN) decreases fertility of several mammals; however, the mechanisms have not been investigated in mares. We developed an experimental model to elevate BUN, with urea and control treatments (7 mares/treatment), in a crossover design. Urea-treatment consisted of a loading dose of urea (0.03 g/kg of body weight (BW)) and urea injections over 6 hours (0.03 g/kg of BW/h). Control mares received the same volume of saline solution. Blood samples were collected to measure BUN. Uterine and vaginal pH were evaluated after the last intravenous infusion, then endometrial biopsies were collected for RNA-sequencing with a HiSeq 4000. Cuffdiff (2.2.1) was used to identify the differentially expressed genes (DEG) between urea and control groups (false discovery rate-adjusted p-value < 0.1). There was a significant increase in BUN and a decrease of uterine pH in the urea group compared to the control group. A total of 193 genes were DEG between the urea and control groups, with five genes identified as upstream regulators (ETV4, EGF, EHF, IRS2, and SGK1). The DEG were predicted to be related to cell pH, ion homeostasis, changes in epithelial tissue, and solute carriers. Changes in gene expression reveal alterations in endometrial function that could be associated with adverse effects on fertility of mares.
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Project description:At ovulation detection (D0), oral treatment with urea was initiated and continued until D7. Mares received a treatment or control diet (n= 11 mares/group) in a crossover design. The treated group received urea (0.4 g/kg body weight) mixed with sweet feed and molasses, the control group received sweet feed and molasses alone. Blood samples were collected daily, one hour after feeding, for BUN determination. Uterine and vaginal pH were evaluated with an epoxy pH probe. Endometrial biopsies were taken transcervically one hour after the last feeding on D7. RNA sequencing of the endometrium of a subset of mares (n=6/group) was conducted.
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Project description:The aim of the global study was to compare the effects of maternal age and parity on gene expression of equine embryos. For that, 17 embryos were collected at 8 days post ovulation (expanded blastocyst stage) from 3 groups of young or old nulliparous or multiparous mares: 6 from young nulliparous mares (5 or 6 year-old, never foaled before), 5 from young multiparous mares (6 year-old and foaled at least once) and 6 from old multiparous (10-16 year-old and foaled at least once). Embryos collected were cut in 2 parts: one hemi-embryo containing pure trophoblast and the other one containing trophoblast + inner cell mass. ARN extractions were performed for all samples using PicoPure RNA isolation kit (Applied Biosystem). Five nanograms of both parts of each embryo were sequenced in paired-end with a length of 30-50bp separately using Illumina NextSeq 500 High. Data were trimmed using Cutadapt. Sequences with less than 10bp were removed. Data for young and old multiparous mares had been already published in [accession: GSE162893; https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE162893]. Only data for embryos collected from young nulliparous mares are deposited here
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Project description:To better characterize placentitis, we examined the sRNA expression patterns occurring in the endometrium, chorioallantois and serum of mares. Disease was induced in 10 mares via intracervical inoculation of Streptococcus equi ssp. zooepidemicus, either with moderate or high levels of inoculum; three un-inoculated gestationally-matched mares were used as controls. Matched chorioallantois and endometrium were sampled in two locations: region 1 - main lesion by cervical star with placental separation; and region 2 - gross inflammation without placental separation.
2019-07-29 | GSE106398 | GEO
Project description:Nocardioform placentitis (NP) continues to result in episodic outbreaks of abortion and preterm birth in mares and remains a poorly understood disease. The objective of this study was to characterize the transcriptome of the chorioallantois (CA) of mares with NP. Term CA were collected from mares with gross lesions consistent with NP, and NP was subsequently confirmed in four CA based upon pathology and PCR for Amycolatopsis spp. CA samples were collected from the margin of the NP lesion (NPL, n=4) and grossly normal region (NPN, n=4). Additionally, CA samples were collected from normal postpartum mares (Control; CRL, n=4). Transcriptome analysis identified 2,892 DEGs in CRL vs. NPL and 2,450 DEGs in NPN vs. NPL. Functional genomics analysis elucidated that inflammatory signaling, toll-like receptor signaling, inflammasome activation, chemotaxis, and apoptosis pathways dominate NP. The increased leukocytic infiltration in NPL was associated with the upregulation of matrix metalloproteinase (MMP1, MMP3, and MMP8) and apoptosis-related genes, such as caspases (CASP3 and CASP7), which could explain placental separation associated with NP. Also, NP was associated with downregulation of several placenta-regulatory genes (ABCG2, GCM1, EPAS1, and NR3C1), angiogenesis-related genes (VEGFA, FLT1, KDR, and ANGPT2), and glucose transporter coding genes (GLUT1, GLUT10, and GLUT12), as well as upregulation of hypoxia-related genes (HIF1A and EGLN3), which could elucidate placental insufficiency accompanying NP. In conclusion, our findings revealed for the first time, the key regulators and mechanisms underlying placental inflammation, separation, and insufficiency during NP.
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