Role of the EGF receptor in PPARγ-mediated sodium and water transport in human proximal tubule cells

摘要: This study aimed to determine the interaction between EGF receptor (EGFR) and peroxisome proliferator-activated γ (PPARγ) role of EGFR in sodium water transport proximal tubule. Primary human tubule cells (PTCs) were exposed high glucose presence absence pioglitazone. Total phospho-EGFR levels mRNA expression determined by western blot real-time PCR, respectively. Sodium–hydrogen exchanger-3 (NHE3), PPARγ aquaporin 1 (AQP1) blot. The was elucidated using tyrosine kinase inhibitor, PKI166. high-glucose conditions specific small interfering (si)RNA. P-EGFR, PPARγ, AQP1 NHE3 production a rat model diabetes (streptozotocin-induced hypertensive Ren-2 transgenic [mRen2]27 rats) controls, with or without pioglitazone treatment, immunohistochemistry. chromatin immunoprecipitation assay, effect on activation luciferase assay. PTCs both increased protein abundance NHE3, PPARγ. Pioglitazone-induced upregulation abolished High-glucose-induced increases decreased siRNA. but not diabetic further treatment. Pioglitazone induced binding promoter subsequent downstream activation. Our data suggest that mediates PPARγ-induced reabsorption via channels inhibition may be therapeutic strategy treatment nephropathy limiting salt retention, which currently restricts use agonists.