PMID- 8569088
OWN - NLM
STAT- MEDLINE
DCOM- 19960301
LR  - 20190725
IS  - 0085-2538 (Print)
IS  - 0085-2538 (Linking)
VI  - 48
IP  - 4
DP  - 1995 Oct
TI  - Activation of nuclear factor-kappa B correlates with MCP-1 expression by human 
      mesangial cells.
PG  - 1263-71
AB  - Emerging evidence suggests that mesangial cell-derived monocyte chemoattractant 
      protein-1 (MCP-1) is a potentially important mediator of glomerular monocyte 
      infiltration. Interleukin-1 beta (IL-1) has been found in glomeruli during 
      inflammation, and is a potent inducer of MCP-1 expression by mesangial cells. 
      Analysis of the promoter region of the human MCP-1 gene demonstrates several 
      putative binding sites for transcription activating factors, including 
      recognition elements for the IL-1-inducible transcription factor, nuclear 
      factor-kappa B (NF-kappa B). This study investigated the role of NF-kappa B in 
      IL-1-induced MCP-1 expression by human mesangial cells. We found that treating 
      mesangial cells with IL-1 resulted in the rapid activation (within 30 min) and 
      nuclear translocation of NF-kappa B. NF-kappa B activation could be blocked by 
      preventing the proteolytic degradation of I kappa B, the cytoplasmic inhibitor of 
      NF-kappa B, with the protease inhibitor tosyl-phe-chloromethylketone (TPCK). 
      Inhibition of NF-kappa B with TPCK correlated with a dose-dependent reduction in 
      IL-1-induced MCP-1 mRNA levels. Conversely, raising intracellular cyclic-AMP 
      levels, or exposing mesangial cells to herbimycin A, treatments that block 
      IL-1-induced MCP-1 mRNA expression, significantly attenuated NF-kappa B 
      activation. Finally, blocking the synthesis of one of the protein subunits of 
      NF-kappa B with an antisense oligonucleotide decreased MCP-1 mRNA levels in 
      response to IL-1. These data suggest that MCP-1 gene transcription may be 
      mediated, in part, by the transcription factor NF-kappa B.
FAU - Rovin, B H
AU  - Rovin BH
AD  - Department of Medicine, Ohio State University School of Medicine, Columbus, USA.
FAU - Dickerson, J A
AU  - Dickerson JA
FAU - Tan, L C
AU  - Tan LC
FAU - Hebert, C A
AU  - Hebert CA
LA  - eng
GR  - R29 DK-46055/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Kidney Int
JT  - Kidney international
JID - 0323470
RN  - 0 (Antioxidants)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-1)
RN  - 0 (NF-kappa B)
RN  - 0 (Oligonucleotides, Antisense)
RN  - 0 (RNA, Messenger)
RN  - 0 (Serine Proteinase Inhibitors)
RN  - 0 (Thiocarbamates)
RN  - 135467-92-4 (prolinedithiocarbamate)
RN  - 402-71-1 (Tosylphenylalanyl Chloromethyl Ketone)
RN  - 9DLQ4CIU6V (Proline)
SB  - IM
MH  - Antioxidants/pharmacology
MH  - Base Sequence
MH  - Cells, Cultured
MH  - Chemokine CCL2/*genetics
MH  - Gene Expression/drug effects
MH  - Glomerular Mesangium/drug effects/*metabolism
MH  - Humans
MH  - Interleukin-1/pharmacology
MH  - Molecular Sequence Data
MH  - NF-kappa B/genetics/*metabolism
MH  - Oligonucleotides, Antisense/genetics/pharmacology
MH  - Proline/analogs & derivatives/pharmacology
MH  - RNA, Messenger/genetics/metabolism
MH  - Serine Proteinase Inhibitors/pharmacology
MH  - Thiocarbamates/pharmacology
MH  - Tosylphenylalanyl Chloromethyl Ketone/pharmacology
EDAT- 1995/10/01 00:00
MHDA- 1995/10/01 00:01
CRDT- 1995/10/01 00:00
PHST- 1995/10/01 00:00 [pubmed]
PHST- 1995/10/01 00:01 [medline]
PHST- 1995/10/01 00:00 [entrez]
AID - S0085-2538(15)59182-5 [pii]
AID - 10.1038/ki.1995.410 [doi]
PST - ppublish
SO  - Kidney Int. 1995 Oct;48(4):1263-71. doi: 10.1038/ki.1995.410.