Abstract
The aim of this study was to investigate the effect of PPARγ modulation on expression of NHE3 and Na, K-ATPase in PTEC and the potential role of nitric oxide and superoxide anion. PTEC were treated for 4 hours with PPAR ligands (rosiglitazone and 15-deoxy PGJ2) or antagonists (GW9662 and BADGE) and protein expression analyzed by immunoblotting. Also, specific inhibition of NO production using L-NAME and superoxide formation using apocynin was used during incubation with agonists/antagonists. Results showed ~ 25% increase in both NHE3 and Na, K-ATPase expression in cells treated with PPARγ antagonists. PPARγ ligands tended to decrease expression of both transporters. Co-incubation with apocynin resulted in no change in the pattern of response of NHE3 and Na,K, ATPase protein expression while L-NAME addition to PTEC totally abolished the changes in Na,K ATPase expression, while having no effect on NHE3. To identify whether agonists and antagonists have a PPARγ dependent effect, the latter was knocked down in PTEC by transient transfection with siRNA for PPARγ. In the transfected cells, both pioglitazone and rosiglitazone had no effect on protein expression of both sodium transporters indicating a PPARγ mediated response for the ligands. Reduced PPARγ activity in vivo may have an important role in increased tubular Na reabsorption associated with hypertension.
Published Version
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