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Hepatic flavin‐containing monooxygenase gene regulation in different mouse inflammation models
Author(s) -
Zhang Jun,
Chaluvadi Madhusudana,
Reddy Rob,
Motika Meike S,
Cashman John R,
Morgan Edward T
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.2_supplement.651
Subject(s) - tlr4 , monooxygenase , inflammation , lipopolysaccharide , western blot , gene , microbiology and biotechnology , chemistry , gene expression , biology , biochemistry , immunology , cytochrome p450 , enzyme
The objective of the study was to investigate the regulation of hepatic flavin‐containing monooxygenases (FMO) 1, 3, 4, and 5 in mouse models of inflammation, including treatment with Citrobacter rodentrium (Cit), lipopolysaccharide (LPS), and dextran sulfate sodium (DSS). Quantitative real‐time RT‐PCR was used to evaluate the steady state mRNA levels for the various FMO isoforms in these mouse models of inflammation during different treatment time courses. FMO3 was most significantly down‐regulated in Cit treated female mice. FMO1, 3 and 5 were found to be down‐regulated in LPS models. The regulation of hepatic FMO3 protein during Cit treatment was confirmed with Western blot analysis of treated animal liver microsomes. Toll‐like receptor (TLR) 4 is known to be responsible for LPS signaling in association with several proteins. To investigate if TLR4 was responsible for regulation of FMO genes in both LPS and Cit animal models, FMO mRNA levels in female wild‐type (C3H/HeOuJ) and TLR4 mutant (C3H/HeJ) mice were compared in both inflammatory models by real‐time RT‐PCR. The results showed that TLR4 is likely to play only a partial role in FMO3 gene regulation during mice inflammatory response post Cit infection. Supported by NIH grants DK59618 (JRC) and DK072372 (ETM).