scholarly journals Toxic Effects of Fumonisin in Mouse Liver Are Independent of the Peroxisome Proliferator-Activated Receptor α

2005 ◽  
Vol 89 (1) ◽  
pp. 108-119 ◽  
Author(s):  
Kenneth A. Voss ◽  
Jie Liu ◽  
Steven P. Anderson ◽  
Corrie Dunn ◽  
J. David Miller ◽  
...  
Keyword(s):  
Mouse Liver ◽  
Toxic Effects ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor

scholarly journals A meta-analysis study of gene expression datasets in mouse liver under PPARα knockout

2013 ◽  
Vol 95 (2-3) ◽  
pp. 78-88 ◽  
Author(s):  
KAN HE ◽  
ZHEN WANG ◽  
QISHAN WANG ◽  
YUCHUN PAN
Keyword(s):  
Gene Expression ◽  
Mouse Liver ◽  
Meta Analysis ◽  
Expression Patterns ◽  
Hepatic Tissue ◽  
Marker Genes ◽  
Specific Marker ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Microarray Datasets

SummaryGene expression profiling of peroxisome-proliferator-activated receptor α (PPARα) has been used in several studies, but there were no consistent results on gene expression patterns involved in PPARα activation in genome-wide due to different sample sizes or platforms. Here, we employed two published microarray datasets both PPARα dependent in mouse liver and applied meta-analysis on them to increase the power of the identification of differentially expressed genes and significantly enriched pathways. As a result, we have improved the concordance in identifying many biological mechanisms involved in PPARα activation. We suggest that our analysis not only leads to more identified genes by combining datasets from different resources together, but also provides some novel hepatic tissue-specific marker genes related to PPARα according to our re-analysis.

scholarly journals Deoxynivalenol Exposure Suppresses Adipogenesis by Inhibiting the Expression of Peroxisome Proliferator-Activated Receptor Gamma 2 (PPARγ2) in 3T3-L1 Cells

2020 ◽  
Vol 21 (17) ◽  
pp. 6300
Author(s):  
Yurong Zhao ◽  
Shulin Tang ◽  
Ruqin Lin ◽  
Ting Zheng ◽  
Danyang Li ◽  
...  
Keyword(s):  
Cell Model ◽  
Toxic Effects ◽  
Marker Genes ◽  
Peroxisome Proliferator ◽  
Trichothecene Mycotoxin ◽  
Peroxisome Proliferator Activated Receptor ◽  
Histone 3 ◽  
Toxicological Mechanism ◽  
Late Stages ◽  
Adipogenic Marker

Deoxynivalenol (DON)—a type B trichothecene mycotoxin, mainly produced by the secondary metabolism of Fusarium—has toxic effects on animals and humans. Although DON’s toxicity in many organs including the adrenal glands, thymus, stomach, spleen, and colon has been addressed, its effects on adipocytes have not been investigated. In this study, 3T3-L1 cells were chosen as the cell model and treated with less toxic doses of DON (100 ng/mL) for 7 days. An inhibition of adipogenesis and decrease in triglycerides (TGs) were observed. DON exposure significantly downregulated the expression of PPARγ2 and C/EBPα, along with that of other adipogenic marker genes in 3T3-L1 cells and BALB/c mice. The anti-adipogenesis effect of DON and the downregulation of the expression of adipogenic marker genes were effectively reversed by PPARγ2 overexpression. The repression of PPARγ2′s expression is the pivotal event during DON exposure regarding adipogenesis. DON exposure specifically decreased the di-/trimethylation levels of Histone 3 at lysine 4 in 3T3-L1 cells, therefore weakening the enrichment of H3K4me2 and H3K4me3 at the Pparγ2 promoter and suppressing its expression. Conclusively, DON exposure inhibited PPARγ2 expression via decreasing H3K4 methylation, downregulated the expression of PPARγ2-regulated adipogenic marker genes, and consequently suppressed the intermediate and late stages of adipogenesis. Our results broaden the current understanding of DON’s toxic effects and provide a reference for addressing the toxicological mechanism of DON’s interference with lipid homeostasis.

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