PMID- 12124772
OWN - NLM
STAT- MEDLINE
DCOM- 20020823
LR  - 20220129
IS  - 0021-9541 (Print)
IS  - 0021-9541 (Linking)
VI  - 192
IP  - 3
DP  - 2002 Sep
TI  - Antagonistic effect of NK4 on HGF/SF induced changes in the transendothelial 
      resistance (TER) and paracellular permeability of human vascular endothelial 
      cells.
PG  - 268-75
AB  - Hepatocyte growth factor/scatter factor (HGF/SF) is a multi-function cytokine 
      that has been shown to regulate the expression of cell adhesion molecules in 
      human endothelial cells. It is also a key cytokine in the development and 
      progression of cancer, particularly during metastasis. NK4 is a variant of HGF/SF 
      that has already been shown to be antagonistic to HGF/SF. This study shows that 
      HGF/SF decreased transendothelial resistance (TER) and increased paracellular 
      permeability in human vascular endothelial cells can that such effects can be 
      inhibited by addition of the NK4 variant. In addition, HGF/SF-stimulated invasion 
      of endothelium by breast cancer cells was inhibited by the addition of NK4. 
      Western blotting revealed that HGF/SF decreased the protein level, and increased 
      tyrosine phosphorylation of ZO-1, but did not cause a change in level of occludin 
      or claudin-1, both molecules involved in tight junction function. RT-PCR revealed 
      that addition of HGF/SF caused no change in signal for claudin-5 or junctional 
      adhesion molecule (JAM), but there was a decrease in the signal for claudin-1. 
      NK4 was able to prevent the decrease in levels of ZO-1 protein by HGF/SF.
CI  - Copyright 2002 Wiley-Liss, Inc.
FAU - Martin, Tracey A
AU  - Martin TA
AD  - Metastasis Research Group, University Department of Surgery, University of Wales 
      College of Medicine, Heath Park, Cardiff, United Kingdom. martinta1@cf.ac.uk
FAU - Mansel, Robert E
AU  - Mansel RE
FAU - Jiang, Wen G
AU  - Jiang WG
LA  - eng
GR  - 1999:73/BCN_/Breast Cancer Now/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Cell Physiol
JT  - Journal of cellular physiology
JID - 0050222
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (HGF protein, human)
RN  - 0 (Junctional Adhesion Molecules)
RN  - 0 (Membrane Proteins)
RN  - 0 (Mitogens)
RN  - 0 (Phosphoproteins)
RN  - 0 (TJP1 protein, human)
RN  - 0 (Zonula Occludens-1 Protein)
RN  - 67256-21-7 (Hepatocyte Growth Factor)
SB  - IM
MH  - Breast Neoplasms/blood supply
MH  - Capillary Permeability/drug effects/physiology
MH  - Cell Adhesion Molecules/genetics/physiology
MH  - Cell Membrane Permeability/drug effects/physiology
MH  - Cells, Cultured
MH  - Endothelium, Vascular/*drug effects/*physiology
MH  - Female
MH  - Hepatocyte Growth Factor/*antagonists & inhibitors/*pharmacology/physiology
MH  - Humans
MH  - Junctional Adhesion Molecules
MH  - Membrane Proteins/genetics/physiology
MH  - *Mitogens
MH  - Neoplasm Invasiveness
MH  - Neovascularization, Pathologic
MH  - Phosphoproteins/physiology
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Tight Junctions/drug effects/physiology
MH  - Tumor Cells, Cultured
MH  - Zonula Occludens-1 Protein
EDAT- 2002/07/19 10:00
MHDA- 2002/08/24 10:01
CRDT- 2002/07/19 10:00
PHST- 2002/07/19 10:00 [pubmed]
PHST- 2002/08/24 10:01 [medline]
PHST- 2002/07/19 10:00 [entrez]
AID - 10.1002/jcp.10133 [doi]
PST - ppublish
SO  - J Cell Physiol. 2002 Sep;192(3):268-75. doi: 10.1002/jcp.10133.