Downregulation of vascular endothelial growth factor and its receptors in the kidney in rats with puromycin aminonucleoside nephrosis.
AIM: We aimed to examine the possible involvement of vascular endothelial growth factor (VEGF) in the pathogenesis of puromycin aminonucleoside nephrosis (PAN). METHODS: The expression and localization of the mRNA of VEGF and its receptors, flt-1 and flk-1, were analyzed in the kidneys of puromycin aminonucleoside-injected rats by use of Northern blotting and in situ hybridization. RESULTS: In association with the induction of proteinuria, VEGF mRNA underwent decrease in amount from 3 days after the injection, reaching the minimum level at 7 days, followed by a gradual recovery by 28 days. The levels of flk-1 and flt-1 mRNA showed similar transient decrease in PAN kidney, whereas the mRNA of von Willebrand factor, a marker of endothelial cells, showed no change in amount. In the normal rat kidney, VEGF mRNA was localized primarily to podocytes, and flk-1 mRNA was localized exclusively to endothelial cells with much higher intensity in glomeruli than in peritubular capillaries. In PAN kidney, the intensities of both VEGF and flk-1 signals in podocytes and glomerular endothelial cells, respectively, appeared much lower at 7 days than in normal kidney. CONCLUSION: These results indicate that the VEGF- VEGF receptor system is downregulated in PAN, implying that it is not involved in the mechanism of proteinuria in PAN.[1]References
- Downregulation of vascular endothelial growth factor and its receptors in the kidney in rats with puromycin aminonucleoside nephrosis. Fan, L., Wakayama, T., Yokoyama, S., Amano, O., Iseki, S. Nephron (2002) [Pubmed]
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