PMID- 18092944
OWN - NLM
STAT- MEDLINE
DCOM- 20080508
LR  - 20091119
IS  - 1470-8736 (Electronic)
IS  - 0143-5221 (Linking)
VI  - 114
IP  - 10
DP  - 2008 May
TI  - Expression and function of ephrin-B1 and its cognate receptor EphB2 in human 
      atherosclerosis: from an aspect of chemotaxis.
PG  - 643-50
AB  - Although several cytokines and chemokines have been demonstrated to play pivotal 
      roles in the pathophysiological conditions of atherosclerosis, few findings exist 
      regarding the expression and function of cytokine-modulating molecules such as 
      ephrin-Bs and their cognate receptors, EphBs, in human atherosclerosis. 
      Therefore, in the present study, we screened novel genes modulating atherogenesis 
      by cDNA array and quantitatively determined them by real-time RT (reverse 
      transcription)-PCR in human carotid atherosclerotic plaques. Ephrin-B1 and EphB2, 
      key regulators of embryogenesis, were significantly up-regulated in plaques 
      compared with those in adjacent control tissues [ephrin-B1, 0.638+/-0.106 
      compared with 0.831+/-0.152, or 130% (P<0.05); EphB2, 1.296+/-0.281 compared with 
      2.233+/-0.506, or 172% (P<0.05)]. Immunohistological analysis demonstrated that 
      both ephrin-B1 and EphB2 were expressed in macrophages and T-lymphocytes in 
      plaques as well as in monocytes, T-lymphocytes and arterial endothelial cells 
      isolated from healthy adults. Interestingly, the extracellular domains of 
      ephrin-B1 and EphB2, the expression of which were both enhanced in stimulated 
      THP-1 cells, significantly inhibited spontaneous (22.5 and 27.6% respectively; 
      P<0.01) and MCP-1 (monocyte chemoattractant protein-1)-dependent (29.7 and 22.6% 
      respectively; P<0.01) migration of monocytes. In conclusion, these results 
      demonstrate that ephrin-B1 and EphB2 are overexpressed in atherosclerotic tissue 
      and might locally regulate cell migration, possibly through modulating 
      cytokine-related chemotaxic activity; however, the functional role of these 
      molecules in atherogenesis should be investigated further.
FAU - Sakamoto, Aiji
AU  - Sakamoto A
AD  - Division of Biotechnology, National Cardiovascular Center, Osaka, Japan.
FAU - Ishibashi-Ueda, Hatsue
AU  - Ishibashi-Ueda H
FAU - Sugamoto, Yuka
AU  - Sugamoto Y
FAU - Higashikata, Takeo
AU  - Higashikata T
FAU - Miyamoto, Susumu
AU  - Miyamoto S
FAU - Kawashiri, Masa-Aki
AU  - Kawashiri MA
FAU - Yagi, Kunimasa
AU  - Yagi K
FAU - Konno, Tetsuo
AU  - Konno T
FAU - Hayashi, Kenshi
AU  - Hayashi K
FAU - Fujino, Noboru
AU  - Fujino N
FAU - Ino, Hidekazu
AU  - Ino H
FAU - Takeda, Yoshiyu
AU  - Takeda Y
FAU - Yamagishi, Masakazu
AU  - Yamagishi M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Clin Sci (Lond)
JT  - Clinical science (London, England : 1979)
JID - 7905731
RN  - 0 (Ephrin-B1)
RN  - EC 2.7.10.1 (Receptor, EphB2)
SB  - IM
MH  - Carotid Arteries/*metabolism
MH  - Carotid Artery Diseases/*metabolism
MH  - Case-Control Studies
MH  - Chemotaxis, Leukocyte
MH  - Endarterectomy, Carotid
MH  - Endothelial Cells/metabolism
MH  - Ephrin-B1/*genetics/metabolism
MH  - Gene Expression Profiling/methods
MH  - Humans
MH  - Immunohistochemistry
MH  - Macrophages/metabolism
MH  - Male
MH  - Middle Aged
MH  - Oligonucleotide Array Sequence Analysis
MH  - Receptor, EphB2/*genetics/metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction/methods
MH  - T-Lymphocytes/metabolism
MH  - *Up-Regulation
EDAT- 2007/12/21 09:00
MHDA- 2008/05/09 09:00
CRDT- 2007/12/21 09:00
PHST- 2007/12/21 09:00 [pubmed]
PHST- 2008/05/09 09:00 [medline]
PHST- 2007/12/21 09:00 [entrez]
AID - CS20070339 [pii]
AID - 10.1042/CS20070339 [doi]
PST - ppublish
SO  - Clin Sci (Lond). 2008 May;114(10):643-50. doi: 10.1042/CS20070339.