Inhibition of heparin-binding epidermal growth factor-like growth factor increases albuminuria in puromycin aminonucleoside nephrosis.

@article{Khong2000InhibitionOH,
  title={Inhibition of heparin-binding epidermal growth factor-like growth factor increases albuminuria in puromycin aminonucleoside nephrosis.},
  author={T F Khong and Scott A. Fraser and Marina Katerelos and Kathy Paizis and Prudence A. Hill and David A. Power},
  journal={Kidney international},
  year={2000},
  volume={58 3},
  pages={
          1098-107
        }
}
BACKGROUND Our previous work in the acute puromycin aminonucleoside nephrosis (PAN) model has demonstrated up-regulation of heparin-binding epidermal growth factor-like growth factor (HB-EGF) mRNA and protein within glomerular epithelial cells (GECs) prior to the onset of proteinuria. METHODS To determine whether increased HB-EGF expression in the acute PAN model contributes to the pathogenesis of proteinuria, a monoclonal antibody (DE10) was produced against recombinant human HB-EGF… 
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The results open the perspective that EGFR inhibitors are suited as therapeutics to combat crescentic inflammatory glomerulonephritis.
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HB-EGF is produced in the peritoneal cavity and enhances mesothelial cell adhesion and migration.
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The data suggest that increased expression of HB‐EGF and erbB4/HER4 is a response to inflammation in the glomerulus in accelerated anti‐GBM disease, which may be masked by the redundancy in the EGF growth factor family.
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