Aldosterone Reprograms Promoter Methylation To Regulate αENaC Transcription In Collecting Duct.

Aldosterone Reprograms Promoter Methylation To Regulate αENaC Transcription In Collecting Duct. Am J Physiol Renal Physiol. 2013 Aug 7; Authors: Yu Z, Kong Q, Kone BC Abstract Aldosterone increases tubular sodium absorption largely by increasing epithelial Na(+) channel (ENaC) α transcription in collecting duct principal cells. How aldosterone reprograms basal (αENaC) transcription to high-level activity in the collecting duct is incompletely understood. Promoter methylation, a covalent, but reversible epigenetic process, has been implicated in the control of gene expression in health and disease. We investigated the role of promoter methylation/demethyation in epigenetic control of basal and aldosterone-stimulated (αENaC) transcription in mIMCD3 collecting duct cells. Bisulfite treatment and sequencing analysis after treatment of the cells with the DNA methyltransferase (DNMT) inhibitor 5-aza-2'-deoxycytidine (5-Aza-CdR) identified clusters of methylated cytosines (5mC) in a CpG island near the transcription start site of the (αENaC) promoter. 5-Aza-CdR treatment or siRNA-mediated knockdown of DNMT3b or methyl-CpG binding domain protein (MBD)-4 de-repressed basal (αENaC)transcription, indicating that promoter methylation suppresses basal (αENaC) transcription. Aldosterone triggered a time-dependent decrease in 5mC and DNMT3b, and a concurrent enrichment in 5-hydroxymethylcytosine (5hmC) and ten-eleven translocation (...
Source: Am J Physiol Renal P... - Category: Urology & Nephrology Authors: Tags: Am J Physiol Renal Physiol Source Type: research

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