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Transcriptomic Analysis of the Chorioallantois of Mares with Nocardioform Placentitis

ABSTRACT: Transcriptomic Analysis of the Chorioallantois of Mares with Nocardioform Placentitis

PROVIDER: PRJNA646932 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12247922_1.fastq.gz	Fastqsanger.gz
	SRR12247922_2.fastq.gz	Fastqsanger.gz
	SRR12247923_1.fastq.gz	Fastqsanger.gz
	SRR12247923_2.fastq.gz	Fastqsanger.gz
	SRR12247924_1.fastq.gz	Fastqsanger.gz

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Transcriptomic Analysis of the Chorioallantois of Mares with Nocardioform Placentitis

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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