Project description:This experiment was designed to investigate the effect of Fumonisin B1 exposure on liver gene expression in male mice fed a regular diet (Chow group) and in obese mice which were fed a High fat diet (HFD). The Fumonisin B1 was provided through the drinking water.
Project description:Adult (8 week old) female mice from mixed genetic background (Sv129/C57Bl6J) were either treated with water or with FB1 for one month prior to liver gene expression analysis.
Project description:Fumonisin B1 (FB1) is a mycotoxin produced by Fusarium species. In mammals, this toxin causes multiple organ-specific damages. Among its multiple effects, FB1 promotes hepatotoxicity, is immunotoxic and alters the intestinal functions. Despite its inhibitory effect on de novo ceramide synthesis, the molecular mechanism of FB1 action and toxicity remain unclears. In order to explore the mechanism of FB1 toxicity, we analyzed the transcriptome of the spleen.
Project description:Fumonisin B1 (FB1) is a mycotoxin produced by Fusarium species. In mammals, this toxin causes multiple organ-specific damages. Among its multiple effects, FB1 promotes hepatotoxicity, is immunotoxic and alters the intestinal functions. Despite its inhibitory effect on de novo ceramide synthesis, the molecular mechanism of FB1 action and toxicity remain unclears. In order to explore the mechanism of FB1 toxicity, we analyzed the transcriptome of the jejunal section which is targeted by FB1.
Project description:Fumonisin B1 (FB1) is a mycotoxin produced by Fusarium species. In mammals, this toxin causes multiple organ-specific damages. Among its multiple effects, FB1 promotes hepatotoxicity, is immunotoxic and alters the intestinal functions. Despite its inhibitory effect on de novo ceramide synthesis, the molecular mechanism of FB1 action and toxicity remain unclears. In order to explore the mechanism of FB1 toxicity, we analyzed the transcriptome of the liver which is targeted by FB1.
Project description:Fumonisin B1 (FB1) is a mycotoxin produced by Fusarium species. In mammals, this toxin causes multiple organ-specific damages. Among its multiple effects, FB1 promotes hepatotoxicity, is immunotoxic and alters the intestinal functions. Despite its inhibitory effect on de novo ceramide synthesis, the molecular mechanism of FB1 action and toxicity remain unclears. In order to explore the mechanism of FB1 toxicity, we analyzed the transcriptome of the jejunal Peyer's patches.
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.
Project description:Fumonisin B1 (FB1) is a mycotoxin produced by Fusarium species. In mammals, this toxin causes multiple organ-specific damages. Among its multiple effects, FB1 promotes hepatotoxicity, is immunotoxic and alters the intestinal functions. Despite its inhibitory effect on de novo ceramide synthesis, the molecular mechanism of FB1 action and toxicity remain unclears. In order to explore the mechanism of FB1 toxicity in multiple tissues, we analyzed the transcriptome of the jejunal section, liver, spleen and jejunal Peyer's patches which are targeted by FB1.
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.