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Eicosanoid Imbalance in the NOD Mouse Is Related to a Dysregulation in Soluble Epoxide Hydrolase and 15‐PGDH Expression
Author(s) -
RODRIGUEZ MICHELLE,
CLARESALZLER MICHAEL
Publication year - 2006
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1375.019
Subject(s) - eicosanoid , proinflammatory cytokine , nod , epoxide hydrolase 2 , epoxide hydrolase , inflammation , chemistry , leukotriene , leukotriene b4 , lipoxygenase , eicosanoid metabolism , prostaglandin e , cyclooxygenase , prostaglandin , biochemistry , biology , enzyme , arachidonic acid , immunology , microsome , gene , asthma
Eicosanoids promote or resolve inflammation depending on the class produced. Macrophage from nonobese diabetic (NOD) mouse produce increased proinflammatory lipid mediators and low levels of antiinflammatory lipoxin A4 (LXA4). The enhanced proinflammatory eicosanoids is secondary to increased cyclooxygenase‐2 (Cox‐2) expression and low levels of prostaglandin/leukotriene catabolic enzyme, 15‐hydroxyprostaglandin dehydrogenase (15‐PGDH). Deficient LXA4 production is not due to deficient lipoxygenase (LO) activity, but is related to increased soluble epoxide hydrolase (sEH), involved in metabolism of anti‐inflammatory epoxyeicosatrienoic acids (EET). These aberrations in eicosanoid biology suggest that inflammation in the NOD mouse is likely to be prolonged and robust and may contribute to type 1 diabetes (T1D) pathogenesis.