PMID- 23108091
OWN - NLM
STAT- MEDLINE
DCOM- 20130117
LR  - 20211021
IS  - 1521-7035 (Electronic)
IS  - 1521-6616 (Print)
IS  - 1521-6616 (Linking)
VI  - 145
IP  - 3
DP  - 2012 Dec
TI  - Fli-1 transcription factor affects glomerulonephritis development by regulating 
      expression of monocyte chemoattractant protein-1 in endothelial cells in the 
      kidney.
PG  - 201-8
LID - S1521-6616(12)00231-8 [pii]
LID - 10.1016/j.clim.2012.09.006 [doi]
AB  - Expression of transcription factor Fli-1 is implicated in the development of 
      glomerulonephritis. Fli-1 heterozygous knockout (Fli1(+/-)) NZM2410 mice, a 
      murine model of lupus, had significantly improved survival and reduced 
      glomerulonephritis. In this study, we found that infiltrated inflammatory cells 
      were significantly decreased in the kidneys from Fli-1(+/-) NZM2410 mice. The 
      expression of monocyte chemoattractant protein-1 (MCP-1) was significantly 
      decreased in kidneys from Fli-1(+/-) NZM2410 mice. The primary endothelial cells 
      isolated from the kidneys of Fli-1(+/-) NZM2410 mice produced significantly less 
      MCP-1. In endothelial cells transfected with specific Fli-1 siRNA the production 
      of MCP-1 was significantly reduced compared to cells transfected with negative 
      control siRNA. By Chromatin Immunoprecipitation (ChIP) assay, we further 
      demonstrated that Fli-1 directly binds to the promoter of the MCP-1 gene. Our 
      data indicate that Fli-1 impacts glomerulonephritis development by regulating 
      expression of inflammatory chemokine MCP-1 and inflammatory cell infiltration in 
      the kidneys in the NZM2410 mice.
CI  - Published by Elsevier Inc.
FAU - Suzuki, Eiji
AU  - Suzuki E
AD  - Department of Medicine, Division of Rheumatology & Immunology, Medical University 
      of South Carolina, Charleston, SC 29425, USA.
FAU - Karam, Eva
AU  - Karam E
FAU - Williams, Sarah
AU  - Williams S
FAU - Watson, Dennis K
AU  - Watson DK
FAU - Gilkeson, Gary
AU  - Gilkeson G
FAU - Zhang, Xian K
AU  - Zhang XK
LA  - eng
GR  - R01 AR056670/AR/NIAMS NIH HHS/United States
GR  - R01AR056670/AR/NIAMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
DEP - 20120928
PL  - United States
TA  - Clin Immunol
JT  - Clinical immunology (Orlando, Fla.)
JID - 100883537
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Fli1 protein, mouse)
RN  - 0 (Proto-Oncogene Protein c-fli-1)
RN  - 0 (RNA, Small Interfering)
RN  - 9007-49-2 (DNA)
SB  - IM
MH  - Animals
MH  - Base Sequence
MH  - Binding Sites/genetics
MH  - Chemokine CCL2/genetics/*metabolism
MH  - DNA/genetics/metabolism
MH  - Disease Models, Animal
MH  - Endothelial Cells/metabolism
MH  - Gene Expression
MH  - Glomerulonephritis/*etiology/genetics/*metabolism/pathology
MH  - Heterozygote
MH  - Humans
MH  - Kidney/metabolism/pathology
MH  - Lupus Nephritis/etiology/genetics/metabolism/pathology
MH  - Mice
MH  - Mice, Knockout
MH  - Promoter Regions, Genetic
MH  - Proto-Oncogene Protein c-fli-1/antagonists & 
      inhibitors/deficiency/genetics/*metabolism
MH  - RNA, Small Interfering/genetics
PMC - PMC3501541
MID - NIHMS411596
COIS- Conflict of interest statement The authors have no financial conflicts of 
      interest.
EDAT- 2012/10/31 06:00
MHDA- 2013/01/18 06:00
PMCR- 2013/12/01
CRDT- 2012/10/31 06:00
PHST- 2012/04/25 00:00 [received]
PHST- 2012/09/12 00:00 [revised]
PHST- 2012/09/14 00:00 [accepted]
PHST- 2012/10/31 06:00 [entrez]
PHST- 2012/10/31 06:00 [pubmed]
PHST- 2013/01/18 06:00 [medline]
PHST- 2013/12/01 00:00 [pmc-release]
AID - S1521-6616(12)00231-8 [pii]
AID - 10.1016/j.clim.2012.09.006 [doi]
PST - ppublish
SO  - Clin Immunol. 2012 Dec;145(3):201-8. doi: 10.1016/j.clim.2012.09.006. Epub 2012 
      Sep 28.