EPAJ: Effect of mares' parity and age
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ABSTRACT:
PROVIDER: PRJNA797166 | ENA |
REPOSITORIES: ENA
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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: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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