Abstract
The mineralocorticoid aldosterone is a major regulator of sodium (Na+) transport and contributes to the control of blood pressure and cardiac function. We previously used microarray technology to identify the immediate transcriptional targets of aldosterone in a mouse inner medullary collecting duct cell line, mIMCD‐3 (Gumz et al. AJP Renal 2003 285:F664); two of the induced transcripts were circadian clock genes, Per1 and Per2. The goals of the present study were to characterize the transcriptional regulation of Per1 and Per2 by aldosterone and to define the role of Per1 in the aldosterone‐mediated regulation of Na+ transport. We confirmed that aldosterone up‐regulates Per1 and Per2 mRNA in mIMCD‐3 cells as well as a second murine cell line, IMCD‐K2. RNA silencing was used to test the hypothesis that Per1 mediates the downstream effects of aldosterone on Na+ transport. Interestingly, knockdown of Per1 with any of four independent Per1 siRNA sequences dramatically decreased mRNA levels of the alpha subunit of the epithelial Na+ channel (ENaCα) in the presence of aldosterone. Importantly, Per1 knockdown had no effect on the serum and glucocorticoid induced kinase 1 (Sgk1) mRNA levels. These data indicate that Per1 plays a role in the aldosterone‐mediated regulation of Na+ transport via ENaCα, and this effect appears to be independent of Sgk1.
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