PMID- 9573530
OWN - NLM
STAT- MEDLINE
DCOM- 19980630
LR  - 20141120
IS  - 0085-2538 (Print)
IS  - 0085-2538 (Linking)
VI  - 53
IP  - 5
DP  - 1998 May
TI  - Heparin-binding epidermal growth factor-like growth factor in experimental models 
      of membranous and minimal change nephropathy.
PG  - 1162-71
AB  - Heparin-binding epidermal growth factor-like growth factor (HB-EGF) is a recently 
      described member of the epidermal growth factor (EGF) family. It binds to heparan 
      sulfate proteoglycans via a cationic domain and is a potent mitogen for 
      epithelial cells, fibroblasts and vascular smooth muscle cells. In the present 
      study we have attempted to identify changes in quantity and distribution of 
      HB-EGF in two models of acute glomerular epithelial cell injury, using Western 
      blotting, immunohistochemistry and in situ hybridization. Prior to disease 
      induction, Western blots showed some expression of HB-EGF protein within 
      glomeruli. Within the first three days in the acute puromycin aminonucleoside 
      (PAN) and passive Heymann nephritis (PHN) models, immunohistochemistry and in 
      situ hybridization demonstrated an up-regulation of HB-EGF mRNA and protein in 
      glomerular epithelial cells (GEC). In both cases, increased protein and mRNA was 
      found prior to the onset of proteinuria and continued until day 21 
      post-induction, the last time point studied. Early in the course of the models, 
      HB-EGF was localized to the cytoplasm of glomerular epithelial cells. At day 21, 
      however, HB-EGF protein was distributed in a nodular pattern within GEC and along 
      the glomerular basement membrane (GBM) in both models, suggesting that the 
      secreted form might bind to the membrane. The increase in HB-EGF protein within 
      glomeruli was confirmed by Western blots of glomerular membrane protein which, 
      however, demonstrated a single 29 kDa species, consistent with the transmembrane 
      form. These data are not consistent with binding of the secreted form of HB-EGF 
      to the GBM. The transmembrane form of HB-EGF is able to signal in a juxtracrine 
      fashion, so increased expression of HB-EGF mRNA and protein by GEC might 
      contribute to the genesis of proteinuria through the initiation of abortive GEC 
      mitogenesis.
FAU - Paizis, K
AU  - Paizis K
AD  - Department of Clinical Immunology, St. Vincent's Hospital, Fitzroy, Victoria, 
      Australia.
FAU - Kirkland, G
AU  - Kirkland G
FAU - Polihronis, M
AU  - Polihronis M
FAU - Katerelos, M
AU  - Katerelos M
FAU - Kanellis, J
AU  - Kanellis J
FAU - Power, D A
AU  - Power DA
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Kidney Int
JT  - Kidney international
JID - 0323470
RN  - 0 (Hbegf protein, rat)
RN  - 0 (Heparin-binding EGF-like Growth Factor)
RN  - 0 (Intercellular Signaling Peptides and Proteins)
RN  - 0 (RNA, Messenger)
RN  - 62229-50-9 (Epidermal Growth Factor)
SB  - IM
MH  - Amino Acid Sequence
MH  - Animals
MH  - Blotting, Western
MH  - Disease Models, Animal
MH  - Epidermal Growth Factor/chemistry/genetics/*metabolism
MH  - Glomerulonephritis, Membranous/genetics/*metabolism/pathology
MH  - Heparin-binding EGF-like Growth Factor
MH  - Immunohistochemistry
MH  - In Situ Hybridization
MH  - Intercellular Signaling Peptides and Proteins
MH  - Male
MH  - Molecular Sequence Data
MH  - Nephrosis, Lipoid/genetics/*metabolism/pathology
MH  - RNA, Messenger/genetics/metabolism
MH  - Rabbits
MH  - Rats
MH  - Rats, Sprague-Dawley
EDAT- 1998/05/09 00:00
MHDA- 1998/05/09 00:01
CRDT- 1998/05/09 00:00
PHST- 1998/05/09 00:00 [pubmed]
PHST- 1998/05/09 00:01 [medline]
PHST- 1998/05/09 00:00 [entrez]
AID - S0085-2538(15)30524-X [pii]
AID - 10.1046/j.1523-1755.1998.00846.x [doi]
PST - ppublish
SO  - Kidney Int. 1998 May;53(5):1162-71. doi: 10.1046/j.1523-1755.1998.00846.x.