Differential gene expression in mouse primary hepatocytes exposed to the peroxisome proliferator-activated receptor α agonists
2006

Effects of PPARα Agonists on Gene Expression in Mouse Liver Cells

Sample size: 3 publication 10 minutes Evidence: moderate

Author Information

Author(s): Guo Lei, Fang Hong, Collins Jim, Fan Xiao-hui, Dial Stacey, Wong Alex, Mehta Kshama, Blann Ernice, Shi Leming, Tong Weida, Dragan Yvonne P

Primary Institution: Division of Systems Toxicology, National Center for Toxicological Research, US Food and Drug Administration

Hypothesis

The study investigates the molecular mechanisms responsible for the effects of PPARα agonists on gene expression in mouse primary hepatocytes.

Conclusion

The treatment of PPARα agonists leads to oxidative stress and increased peroxisome proliferation, which may contribute to hepatic disorders and liver cancer.

Supporting Evidence

  • Treatment with PPARα agonists resulted in the regulation of 121 genes commonly affected by at least two drugs.
  • Gene expression profiles showed increased expression of genes involved in fatty acid oxidation and metabolism.
  • Oxidative stress was linked to the carcinogenic potential of PPARα agonists in rodent liver.

Takeaway

When we give certain drugs to mouse liver cells, they change how the cells work, which might make them sick or even cause cancer.

Methodology

Mouse primary hepatocytes were treated with three PPARα agonists at various concentrations, and gene expression was analyzed using microarray technology.

Limitations

The study is limited to mouse primary hepatocytes and may not fully represent human responses.

Participant Demographics

C57/BL6 male mice, aged 6-8 weeks.

Statistical Information

P-Value

p<0.05

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1186/1471-2105-7-S2-S18

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