PMID- 24098442
OWN - NLM
STAT- MEDLINE
DCOM- 20140728
LR  - 20211021
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 8
IP  - 10
DP  - 2013
TI  - A novel role for adipose ephrin-B1 in inflammatory response.
PG  - e76199
LID - 10.1371/journal.pone.0076199 [doi]
LID - e76199
AB  - 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.
FAU - Mori, Takuya
AU  - Mori T
AD  - Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, 
      Suita, Osaka, Japan.
FAU - Maeda, Norikazu
AU  - Maeda N
FAU - Inoue, Kana
AU  - Inoue K
FAU - Sekimoto, Ryohei
AU  - Sekimoto R
FAU - Tsushima, Yu
AU  - Tsushima Y
FAU - Matsuda, Keisuke
AU  - Matsuda K
FAU - Yamaoka, Masaya
AU  - Yamaoka M
FAU - Suganami, Takayoshi
AU  - Suganami T
FAU - Nishizawa, Hitoshi
AU  - Nishizawa H
FAU - Ogawa, Yoshihiro
AU  - Ogawa Y
FAU - Funahashi, Tohru
AU  - Funahashi T
FAU - Shimomura, Iichiro
AU  - Shimomura I
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20131001
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Ephrin-B1)
RN  - 0 (RNA, Messenger)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
SB  - IM
MH  - Adipocytes/metabolism
MH  - Adipose Tissue/*metabolism/pathology
MH  - Animals
MH  - Cell Adhesion/genetics
MH  - Cell Line
MH  - Enzyme Activation
MH  - Ephrin-B1/genetics/*metabolism
MH  - Gene Expression Regulation
MH  - Gene Knockdown Techniques
MH  - Inflammation/genetics/*metabolism
MH  - Male
MH  - Mice
MH  - Mitogen-Activated Protein Kinase 1/metabolism
MH  - Mitogen-Activated Protein Kinase 3/metabolism
MH  - Models, Biological
MH  - Monocytes/metabolism
MH  - Obesity/genetics/metabolism
MH  - Panniculitis/genetics/metabolism
MH  - RNA, Messenger/genetics/metabolism
PMC - PMC3787942
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2013/10/08 06:00
MHDA- 2014/07/30 06:00
PMCR- 2013/10/01
CRDT- 2013/10/08 06:00
PHST- 2013/08/01 00:00 [received]
PHST- 2013/08/20 00:00 [accepted]
PHST- 2013/10/08 06:00 [entrez]
PHST- 2013/10/08 06:00 [pubmed]
PHST- 2014/07/30 06:00 [medline]
PHST- 2013/10/01 00:00 [pmc-release]
AID - PONE-D-13-31773 [pii]
AID - 10.1371/journal.pone.0076199 [doi]
PST - epublish
SO  - PLoS One. 2013 Oct 1;8(10):e76199. doi: 10.1371/journal.pone.0076199. eCollection 
      2013.