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Inflammatory prompts produce isoform‐specific changes in the expression of leukotriene B 4 ω‐hydroxylases in rat liver and kidney
Author(s) -
Kalsotra Auinash,
Cui Xiaoming,
Antonovic Leposava,
Robida Aaron M,
Morgan Edward T,
Strobel Henry W
Publication year - 2003
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(03)01240-7
Subject(s) - cytochrome p450 , in vivo , arachidonic acid , kidney , lipopolysaccharide , endocrinology , gene isoform , medicine , isozyme , chemistry , leukotriene , leukotriene c4 , pharmacology , biology , biochemistry , enzyme , metabolism , gene , microbiology and biotechnology , asthma
Cytochrome P450 (CYP) 4Fs metabolize leukotriene B 4 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. BaSO 4 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.