PMID- 9174597
OWN - NLM
STAT- MEDLINE
DCOM- 19970630
LR  - 20081121
IS  - 0014-2980 (Print)
IS  - 0014-2980 (Linking)
VI  - 27
IP  - 5
DP  - 1997 May
TI  - Cytokine induction of monocyte chemoattractant protein-1 gene expression in human 
      endothelial cells depends on the cooperative action of NF-kappa B and AP-1.
PG  - 1091-7
AB  - Chemokines are potent mediators of cell migration and activation and therefore 
      play an essential role in early events of inflammation. In conjunction with cell 
      adhesion molecules, chemokines help to localize cells to a specific site and 
      enhance the inflammatory reaction at the site. Clinically, elevated levels of 
      chemokines have been found in a variety of inflammatory diseases. The prototype 
      C-C chemokine is monocyte chemoattractant protein-1 (MCP-1) which is synthesized 
      by variety of cell types including endothelial cells in response to a variety of 
      stimuli. MCP-1 is a major chemoattractant for monocytes, T lymphocytes, and 
      basophils. In the present study, we investigated the factors involved in 
      cytokine-induced MCP-1 gene expression in human endothelial cells. We present 
      evidence that the nuclear factor (NF)-kappa B-like binding site and the AP-1 
      binding site located 90 and 68 base pairs upstream of the transcriptional start 
      site, respectively, are required for maximal induction of the human MCP-1 
      promoter by interleukin-(IL)-1 beta. Site-directed mutagenesis or deletion of the 
      NF-kappa B-like site decreased the cytokine-induced activity of the promoter. 
      Site-directed mutagenesis of the AP-1 binding site also decreased the 
      cytokine-induced activity of the promoter. We show that the NF-kappa B-like site 
      located at-90 in the MCP-1 promoter binds to the p50/p65 heterodimer of the 
      NF-kappa B/Rel family in IL-1 beta-stimulated human endothelial cells. 
      Overexpression of p65 results in the transactivation of the MCP-1 promoter as 
      well. The data presented in this study suggest that cytokine-induced MCP-1 gene 
      expression in human endothelial cells depends on the cooperative action of 
      NF-kappa B and AP-1.
FAU - Martin, T
AU  - Martin T
AD  - Department of Biology, Tanabe Research Laboratories, San Diego, CA 92121, USA.
FAU - Cardarelli, P M
AU  - Cardarelli PM
FAU - Parry, G C
AU  - Parry GC
FAU - Felts, K A
AU  - Felts KA
FAU - Cobb, R R
AU  - Cobb RR
LA  - eng
PT  - Journal Article
PL  - Germany
TA  - Eur J Immunol
JT  - European journal of immunology
JID - 1273201
RN  - 0 (Chemokine CCL2)
RN  - 0 (Cytokines)
RN  - 0 (Interleukin-1)
RN  - 0 (NF-kappa B)
RN  - 0 (NF-kappa B p50 Subunit)
RN  - 0 (Proto-Oncogene Proteins)
RN  - 0 (Proto-Oncogene Proteins c-rel)
RN  - 0 (Transcription Factor AP-1)
RN  - 0 (Transcription Factor RelA)
RN  - 0 (Transcription Factors)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Base Sequence
MH  - Cells, Cultured
MH  - Chemokine CCL2/*biosynthesis/*genetics
MH  - Cytokines/*physiology
MH  - Dimerization
MH  - Endothelium, Vascular/*metabolism
MH  - Gene Expression Regulation/*immunology
MH  - Humans
MH  - Interleukin-1/physiology
MH  - Molecular Sequence Data
MH  - NF-kappa B/biosynthesis/metabolism/*physiology
MH  - NF-kappa B p50 Subunit
MH  - Promoter Regions, Genetic/physiology
MH  - Proto-Oncogene Proteins/biosynthesis
MH  - Proto-Oncogene Proteins c-rel
MH  - Transcription Factor AP-1/*physiology
MH  - Transcription Factor RelA
MH  - Transcription Factors/biosynthesis
MH  - Tumor Necrosis Factor-alpha/physiology
MH  - Umbilical Veins/cytology
EDAT- 1997/05/01 00:00
MHDA- 1997/05/01 00:01
CRDT- 1997/05/01 00:00
PHST- 1997/05/01 00:00 [pubmed]
PHST- 1997/05/01 00:01 [medline]
PHST- 1997/05/01 00:00 [entrez]
AID - 10.1002/eji.1830270508 [doi]
PST - ppublish
SO  - Eur J Immunol. 1997 May;27(5):1091-7. doi: 10.1002/eji.1830270508.