| Autor: |
V, Levidiotis, M, Katerleros, S, Fraser, Pg, Tipping, Da, Power |
| Předmět: |
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| Zdroj: |
Nephrology; Oct2000, Vol. 5 Issue 3, pA103, 1p |
| Abstrakt: |
Synthesis of heparin-binding epidermal growth factor-like growth factor (HB-EGF) is increased by podocytes in experimental models of membranous and minimal change glomerulonephritis. To determine whether this also occurs in more inflammatory forms of glomerulonephritis, we examined the expression of HB-EGF in the accelerated anti-GBM model. The model was induced by standard methods and animals sacrificed at day 10. Expression of HB-EGF was demonstrated using immunohistochemistry and Northern blot analysis. A marked increase in HB-EGF protein expression was localised predominantly to podocytes using a polyclonal antibody that detects the transmembrane form of HB-EGF A two-fold increase in the message for HB-EGF was detected using whole kidney RNA extracts (p = 0.04). To determine the function of increased HB-EGF expression, the monoclonal antibody DE10, directed against the secreted form of HB-EGF, was injected intravenously (0.5 mg/100 g body weight) prior to induction of anti-GBM disease. There was, however, no alteration in proteinuria, renal function or histopathology. Similarly, 40 µg of recombinant HB-EGF injected 24 hours after induction of the disease produced no alteration in proteinuria, renal function or histopathology. Although HB-EGF is upregulated in anti-GBM disease, therefore, the secreted form of HB-EGF does not appear to contribute to disease pathogenesis. This suggests that the transmembrane form may be more important in anti-GBM disease or that this is yet another example of the redundancy of cytokine networks. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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