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A Novel Role for Adipose Ephrin-B1 in Inflammatory Response

2013; Public Library of Science; Volume: 8; Issue: 10 Linguagem: Inglês

10.1371/journal.pone.0076199

1932-6203

Takuya Mori, Norikazu Maeda, Kana Inoue, Ryohei Sekimoto, Yu Tsushima, Keisuke Matsuda, Masaya Yamaoka, Takayoshi Suganami, Hitoshi Nishizawa, Yoshihiro Ogawa, Tohru Funahashi, Iichiro Shimomura,

Biomarkers in Disease Mechanisms

AimsEphrin-B1 (EfnB1) was selected among genes of unknown function in adipocytes or adipose tissue and subjected to thorough analysis to understand its role in the development of obesity. Methods and ResultsEfnB1 mRNA and protein levels were significantly decreased in adipose tissues of obese mice and such reduction was mainly observed in mature adipocytes. Exposure of 3T3-L1 adipocytes to tumor necrosis factor-α (TNF-α) and their culture with RAW264.7 cells reduced EFNB1 levels. Knockdown of adipose EFNB1 increased monocyte chemoattractant protein-1 (Mcp-1) mRNA level and augmented the TNF-α-mediated THP-1 monocyte adhesion to adipocytes. Adenovirus-mediated adipose EFNB1-overexpression significantly reduced the increase in Mcp-1 mRNA level induced by coculture of 3T3-L1 adipocytes with RAW264.7 cells. Monocyte adherent assay showed that adipose EfnB1-overexpression significantly decreased the increase of monocyte adhesion by coculture with RAW264.7 cells. TNF-α-induced activation of extracellular signal-regulated kinase 1/2 (ERK1/2) was reduced by EFNB1-overexpression. ConclusionsEFNB1 contributes to the suppression of adipose inflammatory response. In obesity, reduction of adipose EFNB1 may accelerate the vicious cycle involved in adipose tissue inflammation.