| First Author | Mori T | Year | 2013 |
| Journal | PLoS One | Volume | 8 |
| Issue | 10 | Pages | e76199 |
| PubMed ID | 24098442 | Mgi Jnum | J:337039 |
| Mgi Id | MGI:6238936 | Doi | 10.1371/journal.pone.0076199 |
| Citation | Mori T, et al. (2013) A novel role for adipose ephrin-B1 in inflammatory response. PLoS One 8(10):e76199 |
| abstractText | AIMS: Ephrin-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 RESULTS: EfnB1 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-alpha (TNF-alpha) 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-alpha-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-alpha-induced activation of extracellular signal-regulated kinase 1/2 (ERK1/2) was reduced by EFNB1-overexpression. CONCLUSIONS: EFNB1 contributes to the suppression of adipose inflammatory response. In obesity, reduction of adipose EFNB1 may accelerate the vicious cycle involved in adipose tissue inflammation. |
