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12/15 lipoxygenase products 12(S)HETE and 15(S)HETE induce a proinflammatory response in cultured adipocytes
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.22.1_supplement.1099.5
Subject(s) - proinflammatory cytokine , hydroxyeicosatetraenoic acid , endocrinology , inflammation , medicine , tumor necrosis factor alpha , monocyte , chemistry , lipoxygenase , adipose tissue , biology , biochemistry , enzyme
The 12/15lipoxygenase products 12‐(S)‐hydroxyeicosatetraenoic acid (12‐HETE) and 15‐(S)‐hydroxyeicosatetraenoic acid (15‐HETE) induce inflammatory responses in various cell lines by stimulating the production of proinflammatory cytokines and monocyte chemoattractant proteins (MCP). Furthermore, the production of MCP1 and proinflammatory cytokines by the adipocyte, is pivotal in mediating the chronic inflammatory state associated with obesity and insulin resistance. Therefore, we hypothesized that treatments with 1×10‐7 M 12‐HETE or 15‐HETE would activate inflammatory pathways in 3T3‐L1 adipocytes. The inflammatory mediators (TNF[alpha], IL6 and MCP1) were assessed by RT‐ PCR and media MCP1 protein was measured by ELISA. Treatment with 12‐HETE produced a 1.64 fold increase in TNF[alpha] gene expression versus control (P< 0.01), but failed to alter MCP1 mRNA expression or media protein. However, 15‐HETE caused a significant increase in media MCP1 protein (P<0.01), but only a modest increase in TNF[alpha] gene expression (P= 0.07). IL6 gene expression was not altered with either treatment. These data suggest that 12‐HETE contributes to inflammation by stimulating the production of TNF[alpha] and that 15‐HETE likely facilitates the recruitment of monocytes to the adipose tissue by upregulating the production of MCP1.