Project name: Mus musculus

Description: Aldosterone is arguably the single most important hormone implicated in the control of blood pressure and extracellular fluid volume in mammals. It acts primarily by increasing the rate of transepithelial sodium transport in the kidney tubules. Several monogenetic defects resulting in hypertension have now been attributed to abnormalities in sodium handling within the aldosterone-sensitive distal nephron, where the epithelial sodium channel, ENaC, constitutes the rate-limiting step of sodium transport. To date, the transcription-dependent aldosterone-signaling pathway between receptor and membrane transport effectors, remains incompletely understood. The broad aim of our study is to explore these intracellular signaling pathways that are critical to the functioning of sodium channels. Microarray analysis in an aldosterone-responsive kidney cortical collecting duct cell line (mpkCCDc14), allowed us to identify many potential aldosterone-regulated transcripts. The present study describes the identification, and possible physiological relevance of various aldosterone-regulated transcripts. The results of this study promise to extend our understanding of the molecular basis of aldosterone-regulated sodium transport in kidney epithelia, and provide approaches for regulating this process in disease states such as congestive heart failure and hypertension.Keywords: hormone effectOverall design: mpkCCD Cells were treated with 10-6M aldosterin or ethanol for 1 or 6 hrs. Total RNAs were then isolated and cDNA was made and purified and recovered. The Cy3 or Cy5 was then coupled with cDNA from control or drug-treated cells, respectively. The labeled cDNA was hybridized with microarray slides. 4 arrays for each experimental conditions.

Data type: Transcriptome or Gene expression

Sample scope: Multiisolate

Relevance: ModelOrganism

Release date: 2005-07-15

Last updated: 2005-07-13