Identification of novel aldosterone targets in mouse kidney cortical collecting duct cells (744.1)

Abstract

The kidney is critical for the regulation of blood pressure by maintaining sodium and fluid homeostasis. The hormone aldosterone is critical for the regulation of these processes. Aldosterone acts on principal cells of the renal collecting duct to increase sodium reabsorption by increasing transcription of the epithelial sodium channel and SGK1; these effects are mediated by the mineralocorticoid receptor (MR). Recent work by others identified two novel factors that may play a role in sodium reabsorption in the kidney. FK506 binding protein 5 (FKBP5), a member of the immunophilin family, is a co‐chaperone for MR, and causes increased translocation of MR into the nucleus. Growth arrest‐specific 5 (Gas5) is a long noncoding RNA (lncRNA) that acts as a decoy to the hormone response element (HRE) of MR. Gas5 may compete for binding of MR to the HREs of aldosterone target genes. However, it is unknown if FKBP5 or Gas5 are aldosterone targets. Thus we treated mouse kidney collecting duct cells (mpkCCDc14), with aldosterone for 24 hours. Aldosterone treatment led to increases in FKBP5 and Gas5 RNA expression. These data demonstrate that FKBP5 and Gas5 are potential aldosterone targets in kidney cortical collecting duct cells. This may be the first report demonstrating aldosterone‐mediated regulation of a lncRNA.Grant Funding Source: Supported by NIH, ASN and AHA