Inflammatory prompts produce isoform-specific changes in the expression of leukotriene B4 ω-hydroxylases in rat liver and kidney

Auinash Kalsotra, Xiaoming Cui, Leposava Antonovic, Aaron M. Robida, Edward T. Morgan, Henry W. Strobel

Research output: Contribution to journalArticlepeer-review

Abstract

Cytochrome P450 (CYP) 4Fs metabolize leukotriene B4 and other inflammatory mediators in the arachidonic acid cascade. Here we show that lipopolysaccharide (LPS) treatment suppresses CYP4F4 and up-regulates CYP4F5 mRNA expression in rat liver whereas renal CYP4Fs are essentially unchanged. BaSO4 treatment, in contrast, increases both hepatic and renal CYP4F expression levels. Thus, distinct regulatory mechanisms in CYP4F expression might operate under different inflammatory prompts. To examine hepatic totipotency, primary hepatocytes were treated with varying doses of LPS resulting in decrease in all the CYP4F isoforms. Treatment of hepatocytes with 5 ng/ml of interleukin-1β mimics the in vivo effects of LPS on CYP4F expression.

Original languageEnglish (US)
Pages (from-to)236-242
Number of pages7
JournalFEBS Letters
Volume555
Issue number2
DOIs
StatePublished - Dec 4 2003
Externally publishedYes

Keywords

  • Chlorpromazine metabolism
  • Cytochrome P450 4F
  • Inflammation
  • Interleukin-1
  • Leukotriene B ω-hydroxylase
  • Lipopolysaccharide

ASJC Scopus subject areas

  • Biophysics
  • Structural Biology
  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology

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