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Interplay of Epoxides and Heme Oxygenase System Suppress Adipogenic Regulators in Mesenchymal Stem Cell Derived Adipocytes
Author(s) -
Vanella Luca,
Abraham Nader G
Publication year - 2012
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.26.1_supplement.1121.2
Subject(s) - adipogenesis , chemistry , mesenchymal stem cell , epoxygenase , adiponectin , endocrinology , medicine , agonist , 3t3 l1 , adipocyte , adipose tissue , heme oxygenase , epoxide hydrolase 2 , microbiology and biotechnology , biochemistry , heme , biology , arachidonic acid , insulin resistance , receptor , insulin , enzyme
Epoxygenase activity and synthesis of epoxyeicosatrienoic acids (EETs) have emerged as important modulators of obesity and diabetes. We examined the effect of the EET‐agonist 12‐(3‐ hexylureido)dodec‐8(2) enoic acid on Mesenchymal Stem Cell (MSC) derived adipocytes proliferation and differentiation. MSCs expressed substantial levels of EETs and inhibition of soluble Epoxide Hydrolase (sEH) increased the level of EETs and decreased adipogenesis. EET agonist treatment increased HO‐1 expression by inhibiting a negative regulator of HO‐1 expression, Bach‐1. EET treatment also increased catenin and pACC levels while decreasing PPAR C/EBP and fatty acid synthase levels. These changes were manifest by a decrease in the number of large inflammatory adipocytes, TNF, IFN and IL‐1, but an increase in small adipocytes and in adiponectin levels. In summary, EET agonist treatment inhibits adipogenesis and decreases the levels of inflammatory cytokines suggesting the potential action of EETs as intracellular lipid signaling modulators of adipogenesis and adiponectin. NIH‐ DK056601