Journal
NEPHROLOGY DIALYSIS TRANSPLANTATION
Volume 24, Issue 9, Pages 2637-2645Publisher
OXFORD UNIV PRESS
DOI: 10.1093/ndt/gfp182
Keywords
glomerular basement membrane; heparan sulfate; heparanase; proteinuria; renin-angiotensin-aldosterone system
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Funding
- Dutch Diabetes Research Foundation [2001.00.048]
- Dutch Kidney Foundation [C05.2152]
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Methods. Six weeks after the induction of AN, rats were treated with vehicle (n = 8), lisinopril (75 mg/L, n = 10), spironolactone (3.3 mg/day, n = 12) or the combination of lisinopril and spironolactone (n = 14) for 12 weeks. Age-matched healthy rats served as controls (n = 6). After 18 weeks, renal heparanase and heparan sulfate (HS) expression were examined by immunofluorescence staining. In addition, the effect of aldosterone, AngII and ROS on heparanase expression in cultured podocytes was determined. Results. Treatment with lisinopril, spironolactone or their combination significantly blunted the increased glomerular heparanase expression and restored the decreased HS expression in the GBM. Addition of aldosterone to cultured podocytes resulted in a significantly increased heparanase mRNA and protein expression, which could be inhibited by spironolactone. Heparanase mRNA and protein expression in podocytes were also significantly increased after stimulation with AngII or ROS. Conclusions. Our in vivo and in vitro results show that not only AngII and ROS, but also aldosterone is involved in the regulation of glomerular heparanase expression.
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