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
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.
Project description:The study collected eight mares with chronic endometritis and eight healthy mares, respectively. In LC-MS analysis, the DDA method was employed to identify quantitatively differential proteins.
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
Project description:In order to systematically analyze the maternal, i.e. the endometrial, changes in the equine endometrium underlying the complex embryo-maternal dialogue during early pregnancy, a transcriptome study of endometrium samples from five mares at day 8 and six mares at day 12 of early pregnancy and the corresponding non-pregnant stage was performed. Endometrial biopsies were taken from six warmblood mares at day 12 of early pregnancy after embryo recovery and at the corresponding non-pregnant stage. 12 samples were analyzed: one pregnant sample and the corresponding control sample of every mare each at a time. Endometrial biopsies were taken from five warmblood mares at day 8 of early pregnancy after embryo recovery and at the corresponding non-pregnant stage. 10 samples were analyzed: one pregnant sample and the corresponding control sample of every mare each at a time. Two experimental groups: 8 and 12 days
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.
Project description:In order to systematically analyze the maternal, i.e. the endometrial, changes in the equine endometrium underlying the complex embryo-maternal dialogue during early pregnancy, a transcriptome study of endometrium samples from mares at day 16 of pregnancy and day 12 cyclic mares was performed. Results were compared to a previous study of samples from day 12 of pregnancy and day 12 cyclic controls. Endometrial biopsies were taken from six wormblood mares at day 16 of early pregnancy after embryo recovery and day 12 cyclic controls. 8 samples were analyzed: one pregnant sample and the corresponding control sample of every mare each at a time.
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.