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Transcriptomic and chromatin accessibility analyses of porcine alveolar macrophages exposed to Fumonisin B1

ABSTRACT: Transcriptomic and chromatin accessibility analyses of porcine alveolar macrophages exposed to Fumonisin B1

PROVIDER: PRJNA786598 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17144007_1.fastq.gz	Fastqsanger.gz
	SRR17144007_2.fastq.gz	Fastqsanger.gz
	SRR17144008_1.fastq.gz	Fastqsanger.gz
	SRR17144008_2.fastq.gz	Fastqsanger.gz
	SRR17144009_1.fastq.gz	Fastqsanger.gz

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Transcriptomic and chromatin accessibility analyses of porcine alveolar macrophages exposed to Fumonisin B1

Project description:Fumonisin B1 (FB1) is a mycotoxin that poses a great threat to agricultural production and human and animal health. However, the molecular mechanism underlying the cytotoxic effect of FB1 to mammals has not been systematically elucidated. Here, we utilized the porcine alveolar macrophage cell line 3D4/21 as model, and applied RNA sequencing (RNA-seq) to analyze the genome-wide transcriptional alterations of mRNA, lncRNA, circRNA and miRNA before and after exposure to FB1 in six samples. To further reveal the underlying regulatory mechanism, we applied Assay for Transposase-Accessible Chromatin with high-throughput sequencing (ATAC-seq) to determine the genome-wide chromatin accessibility alterations in response to FB1-induced cytotoxicity. We anticipate that this dataset will serve as valuable resource for clarifying the transcriptional and regulatory mechanism underlying the cytotoxic effect of FB1, and facilitate the identification of the key genes and signaling pathways contributing to cellular response to FB1 exposure.

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Project description:Obesity promotes Fumonisin B1 toxicity and induces hepatitis

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Differential gene expression of Arabidopsis in response to fumonisin B1 and exogenous ATP treatments

Project description:To identify genes underpinning the antagonistic effects of extracellular ATP on programmed cell death induced by fumonisin B1 (FB1), we conducted a kinetic DNA microarray experiment using samples harvested in the critical time window when exogenous ATP is known to suppress cell death. Arabidopsis cell suspension cultures were treated with FB1 at time = 0 h and exogenous ATP added at time = 40 h. Differential gene expression analysis using microarrays was performed on samples harvested at 41, 42, 44, and 48 h.

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Project description:Integrins are extracellular matrix receptors comprised of an a and b subunit that connect and mediate signaling between cells and the surrounding matrix. In organogenesis of epithelial tissues, the b1 integrin subunit regulates essential epithelial cell functions, but the role of b1 integrin in epithelial repair is poorly understood. To define the role of b1 integrin during alveolar repair, we challenged b1 integrin deficient mice with intratracheal lipopolysaccharide, resulting in increased mortality with emphysematous lungs 21 days following injury. The alveolar barrier was repopulated with an overabundance of type 2 alveolar epithelial cells, with reduced numbers of elongated alveolar type 1 cells, suggesting b1 integrin is required for type 2 to type 1 epithelial transition. Consistent with this finding, b1 deficient type 2 epithelial cells proliferated at increased rates throughout repair, lacked actin-rich cellular protrusions necessary for lateral cellular extension, and exhibited transcriptomic dysregulation of adherens junction and actin polymerization pathways. Finally, we show that b1 integrin balances actin polymerization versus stabilization through GTPase activation. Taken together, these data support a novel role for b1 integrin in re-establishing the alveolar niche after injury through modulation of type 2 epithelial cell proliferation and cytoskeletal-dependent cell shape change.

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