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ABSTRACT: RNA-seq of PEDV Infection in IPEC-J2 Cells

PROVIDER: PRJNA991704 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25152682_1.fastq.gz	Fastqsanger.gz
	SRR25152682_2.fastq.gz	Fastqsanger.gz
	SRR25152683_1.fastq.gz	Fastqsanger.gz
	SRR25152683_2.fastq.gz	Fastqsanger.gz
	SRR25152684_1.fastq.gz	Fastqsanger.gz

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Identification of cell types and transcriptome landscapes of PEDV infected porcine small intestine using single-cell RNA-sequencing

Project description:Swine coronavirus-porcine epidemic diarrhea virus (PEDV) with specific susceptibility to pigs has existed for decades, and recurrent epidemics caused by mutant strains have swept the world again since 2010. Here, single-cell RNA-sequencing was used to perform a systematic analysis of pig small intestines infected with PEDV for the first time. Multiple cell types were identified by representative markers, including the unique marker DNAH11 of tuft cells. Meanwhile, the goblet and tuft cells were also susceptible to PEDV except enterocytes. PEDV infection obviously upregulated REG3G, which significantly inhibited virus replication. Notably, IFN-DELTAs in goblet and enterocyte progenitor cells were increased in virus infected piglet, and IFN-DELTA5 could induce GBP1, ISG15, OAS2 and IFITM1 dramatically raised in IPEC-J2 cells and restricted PEDV replication. Complement molecules were mainly expressed in intestinal cells excepting tuft cells, but PEDV decreased C3, C4A, and C5 in enterocytes, thus escaping the antiviral effect of C3. Finally, enterocytes expressed almost all coronavirus entry factors, and PEDV infection caused significant upregulation of the coronavirus receptor ACE2 in porcine enterocyte cells. In summary, this study systematically studied the response of different cell types in small intestine of pigs after PEDV infection, which deepened the understanding of viral pathogenesis.

2022-04-27 | GSE175411 | GEO

Transcriptome-wide m6A methylome of intestinal porcine epithelial cells (IPEC-J2) induced by deoxynivalenol

Project description:Deoxynivalenol (DON) frequently detected in a wide range of foods and feeds, inducing cytotoxicity to animals and humans. N6-methyladenosine (m6A) is an important epitranscriptomic marker with high abundance in eukaryotic mammals mRNAs. However, the role of the m6A methylomes in DON damage is still poorly understood. Here, we investigated the m6A transcriptome-wide profile in intestinal porcine epithelial cells (IPEC-J2) with and without 1000 ng/mL DON treatment via m6A sequencing and RNA sequencing. In total, 5406 new m6A peaks appeared with the disappearance of 2615 peaks in DON-induced IPEC-J2. The unique m6A-modified genes in DON-induced IPEC-J2 were associated with TNF signaling pathway. We identified 733 differentially expressed mRNA transcripts with hyper-methylated or hypo-methylated m6A peaks between DON-induced IPEC-J2 and normal IPEC-J2. Protein interaction network analysis and qPCR validation suggested that CSF2 probably acts as a promising new target for combating DON damage in IPEC-J2. Our first report of m6A transcriptome-wide map of IPEC-J2 cells presented here provides a starting roadmap for uncovering m6A functions that may affect DON infection.

2020-08-13 | GSE156078 | GEO

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Project description:Transcriptome sequencing of IPEC-J2 cells infected with PEDV

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Project description:RNA-seq of IPEC-J2 cells

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Comparing two intestinal porcine epithelial cell lines (IPECs): global expression patterns to characterise a in vitro model of intestinal physiology

Project description:The intestinal epithelial cell lines 1 and J2 (IPEC-1, IPEC-J2) - spontaneously immortalised cell lines from the porcine intestine - are important tools for studying intestinal function. Microarrays (GeneChip Porcine Genome Array) were used to compare the expression pattern at basal in vitro conditions. Expression analyses complemented by morphological, functional and biochemical analyses revealed that IPEC-J2 is a morphologically and functionally more differentiated cell line in comparison to IPEC-1. In addition, IPEC-2 cells are a preferential tool for in vitro studies with the focus on metabolism.

2015-12-31 | GSE67407 | GEO

Sus scrofa

Project description:PEDV infection in IPEC-J2 cells caused the change of circRNA expression pattern

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Project description:RNA-seq of IPEC-J2 cell

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Project description:IVT-SAPAS sequencing of IPEC-J2 cells infected or mock infected PEDV

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4D-DIA proteomics of IPEC-J2 cells infected with porcine group A rotavirus

Project description:IPEC-J2 cells were infected with PoRV AHBZ2304 strain at a multiplicity of infection (MOI) of 1, 24 hours post infection, the cells were subjected to preparation and LC-MS detection and data analysis.

2025-04-20 | PXD063141 |

Comprehensive proteomic analysis reveals omega-3 fatty acids to counteract endotoxin-stimulated metabolic dysregulation in porcine enterocytes

Project description:Omega-3 polyunsaturated fatty acids (n-3 PUFA), such as the eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are reported to beneficially affect intestinal immunity. The intestinal epithelial layer (IEL), made up of absorptive cells as the enterocytes, is the primary site of fatty acid absorption. So far, the biological pathways modulated by n-3 PUFA in IEL during infection remain elusive. In the present study, shotgun proteomics analysis integrated with RNA sequencing (RNA-seq) technology was employed to unveil the proteomic changes induced by n-3 PUFA in enterocytes, in the presence and absence of lipopolysaccharide (LPS) stress conditions. A total of 33, 85, and 88 differential proteins were identified in the IPEC-J2 cells exposed to (i) n-3 PUFA (DHA:EPA, 1:2, 10 µM, 24 h), (ii) LPS (10 µg/mL, 24 h), or (iii) n-3 PUFA pre-treatment followed by LPS stimulation, respectively. Functional annotation and pathway analysis of the differential proteins revealed the modulation of central carbon metabolism, including glycolysis/gluconeogenesis, pentose phosphate pathway, and oxidative phosphorylation. Specifically, LPS caused metabolic dysregulation in the IPEC-J2 cells, abated upon prior treatment with n-3 PUFA. Indeed, n-3 PUFA supplementation facilitated enterocyte development and lipid homeostasis. This work provided a comprehensive picture of the biological pathways modulated by n-3 PUFA in enterocytes, both in the absence and presence of a state of endotoxin-induced metabolic dysregulation. Our findings provide important insights into the role of n-3 PUFA in the intestinal barrier, which could support better planning of nutritional strategies in managing intestinal health and immunity.

2023-12-11 | PXD036456 | Pride

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