PMID- 19426980
OWN - NLM
STAT- MEDLINE
DCOM- 20100119
LR  - 20091109
IS  - 1879-1484 (Electronic)
IS  - 0021-9150 (Linking)
VI  - 207
IP  - 1
DP  - 2009 Nov
TI  - The transcriptional factor PREB mediates MCP-1 transcription induced by cytokines 
      in human vascular endothelial cells.
PG  - 45-50
LID - 10.1016/j.atherosclerosis.2009.03.051 [doi]
AB  - OBJECTIVE: The prolactin regulatory element binding (PREB) protein is a 
      transcriptional factor that regulates prolactin promoter activity in rat anterior 
      pituitary. It is expressed not only in the anterior pituitary but also in the 
      cardiovascular system, including in human umbilical vascular endothelial cells 
      (HUVECs). Monocyte chemoattractant protein-1 (MCP-1) is a major chemotactic 
      factor for monocytes and a key factor initiating the inflammatory process of 
      atherogenesis. MCP-1 is expressed in HUVECs in response to several different 
      stimuli, including interleukin (IL)-1beta and tumor necrosis factor (TNF)-alpha. 
      METHODS AND RESULTS: MCP-1 expression was regulated by IL-1beta and TNF-alpha and 
      cytokine-induced PREB expression. Conversely, over-expression of PREB using a 
      PREB-expressing adenovirus increased MCP-1 expression in HUVECs. In addition, 
      PREB induced the expression of the luciferase reporter protein under the MCP-1 
      promoter control. EMSA showed that the transcriptional effect of PREB was 
      mediated by its binding to the PREB-responsive cis-element of the MCP-1 promoter. 
      Finally, we used siRNA to inhibit PREB expression in HUVECs and demonstrated that 
      knockdown of PREB expression attenuated the effects of IL-1beta and TNF-alpha on 
      MCP-1 expression. CONCLUSIONS: In summary, our findings show that PREB can 
      function as a transcriptional regulator of the MCP-1 promoter in response to 
      cytokines.
FAU - Murao, Koji
AU  - Murao K
AD  - Division of Endocrinology and Metabolism, Department of Internal Medicine, 
      Faculty of Medicine, Kagawa University, 1750-1 Ikenobe Miki-CHO, Kita-gun, Kagawa 
      761-0793, Japan. mkoji@med.kagawa-u.ac.jp
FAU - Imachi, Hitomi
AU  - Imachi H
FAU - Yu, Xiao
AU  - Yu X
FAU - Muraoka, Tomie
AU  - Muraoka T
FAU - Hosami, Naohisa
AU  - Hosami N
FAU - Dobashi, Hiroaki
AU  - Dobashi H
FAU - Ishida, Toshihiko
AU  - Ishida T
LA  - eng
PT  - Journal Article
DEP - 20090411
PL  - Ireland
TA  - Atherosclerosis
JT  - Atherosclerosis
JID - 0242543
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Guanine Nucleotide Exchange Factors)
RN  - 0 (Interleukin-1beta)
RN  - 0 (PREB protein, human)
RN  - 0 (Preb protein, rat)
RN  - 0 (RNA, Messenger)
RN  - 0 (Transcription Factors)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Binding Sites
MH  - Cells, Cultured
MH  - Chemokine CCL2/genetics/*metabolism
MH  - DNA-Binding Proteins/genetics/*metabolism
MH  - Electrophoretic Mobility Shift Assay
MH  - Endothelial Cells/immunology/*metabolism
MH  - Guanine Nucleotide Exchange Factors/genetics/*metabolism
MH  - Humans
MH  - Interleukin-1beta/*metabolism
MH  - Mutation
MH  - Promoter Regions, Genetic
MH  - RNA Interference
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Transcription Factors/genetics/*metabolism
MH  - *Transcriptional Activation
MH  - Transfection
MH  - Tumor Necrosis Factor-alpha/*metabolism
EDAT- 2009/05/12 09:00
MHDA- 2010/01/20 06:00
CRDT- 2009/05/12 09:00
PHST- 2008/10/20 00:00 [received]
PHST- 2009/03/31 00:00 [revised]
PHST- 2009/03/31 00:00 [accepted]
PHST- 2009/05/12 09:00 [entrez]
PHST- 2009/05/12 09:00 [pubmed]
PHST- 2010/01/20 06:00 [medline]
AID - S0021-9150(09)00265-2 [pii]
AID - 10.1016/j.atherosclerosis.2009.03.051 [doi]
PST - ppublish
SO  - Atherosclerosis. 2009 Nov;207(1):45-50. doi: 
      10.1016/j.atherosclerosis.2009.03.051. Epub 2009 Apr 11.