Dataset Information

Sub-chronic testosterone treatment increases the levels of epithelial sodium channel (ENaC)-?, ? and ? in the kidney of orchidectomized adult male Sprague-Dawley rats.

ABSTRACT: Testosterone has been reported to cause blood pressure to increase. However mechanisms that underlie the effect of this hormone on this physiological parameter are currently not well understood. The aims of this study were to investigate effects of testosterone on expression of ?, ? and ?-epithelial sodium channel (ENaC) proteins and messenger RNAs (mRNAs) in kidneys, the channel known to be involved in Na(+) reabsorption, which subsequently can affect the blood pressure. Methods. Adult male Sprague-Dawley (SD) rats were orchidectomized fourteen days prior to receiving seven days treatment with testosterone propionate (125 µg/kg/day or 250 µg/kg/day) with or without flutamide (androgen receptor blocker) or finasteride (5?-reductase inhibitor). Following sacrifice, the kidneys were removed and were subjected for ?, ? and ?-ENaC protein and mRNA expression analyses by Western blotting and Real-time PCR (qPCR) respectively. The distribution of ?, ? and ?-ENaC proteins in kidneys were observed by immunofluorescence. Results. The ?, ? and ?-ENaC proteins and mRNA levels in kidneys were enhanced in rats which received testosterone-only treatment. In these rats, ?, ? and ?-ENaC proteins were distributed in the distal tubules and collecting ducts of the nephrons. Co-treatment with flutamide or finasteride resulted in the levels of ?, ? and ?-ENaC proteins and mRNAs in kidneys to decrease. In conclusions, increases in ?, ? and ?-ENaC protein and mRNA levels in kidneys mainly in the distal tubules and collecting ducts under testosterone influence might lead to enhance Na(+) reabsorption which subsequently might cause an increase in blood pressure.

SUBMITTER: Loh SY

PROVIDER: S-EPMC4933084 | biostudies-literature | 2016

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Sub-chronic testosterone treatment increases the levels of epithelial sodium channel (ENaC)-α, β and γ in the kidney of orchidectomized adult male Sprague-Dawley rats.

Loh Su Yi SY Giribabu Nelli N Salleh Naguib N

PeerJ 20160630

Testosterone has been reported to cause blood pressure to increase. However mechanisms that underlie the effect of this hormone on this physiological parameter are currently not well understood. The aims of this study were to investigate effects of testosterone on expression of α, β and γ-epithelial sodium channel (ENaC) proteins and messenger RNAs (mRNAs) in kidneys, the channel known to be involved in Na(+) reabsorption, which subsequently can affect the blood pressure. Methods. Adult male Spr ...[more]

PMID: 27413634

Similar Datasets

Project description:BackgroundThe amiloride-sensitive Epithelial Sodium Channel (ENaC) is critical in maintaining Na+ balance, extracellular fluid volume and long term blood pressure control. ENaC is composed of three main subunits alpha, beta, & gamma. While alpha ENaC is critical for channel functionality, beta & gamma ENaC maximize channel function. To date, there are four alternatively spliced forms of the alpha subunit of ENaC (alpha ENaC-a, -b, -c, & -d) that have been published in rats, in addition to the major alpha ENaC transcript. While alpha ENaC-a, -c & -d transcripts are low abundance transcripts compared to full-length alpha ENaC, alpha ENaC-b is a higher abundance and salt-sensitive transcript compared to full-length alpha ENaC.Presentation of the hypothesisalpha ENaC-b protein, which is preferentially produced in Dahl R rats, to a greater extent on high salt diet, exerts a dominant negative effect on full-length alpha ENaC subunit by physically binding to and trapping full-length alpha ENaC subunit in the endoplasmic reticulum, and finally accelerating full-length alpha ENaC proteolytic degradation in a dose-dependent manner.Testing the hypothesis1) To examine the mRNA and protein abundance of alpha ENaC-b relative to alpha ENaC full-length in kidney, lung, and taste tissues of Dahl rats. 2) To compare the expression (mRNA and protein) of alpha ENaC-b in kidneys of Dahl S and R rats on regular and high salt diet. 3) To examine the putative binding of alpha ENaC-b proteins to full-length alpha ENaC in vitro and to determine the impact of such binding on full-length alpha ENaC expression in vitro.Implications of the hypothesisOur studies will be the first to demonstrate the over-expression of salt-sensitive alpha ENaC-b spliced form in kidney tissues of Dahl R rats at the expense of full-length alpha ENaC. The current proposal will provide highly novel insights into the putative mechanisms leading to ENaC hypoactivity in high-salt-fed Dahl R rats. Finally, findings from the present proposal will uncover a new mechanism by which alternative splicing may control the regulation of ENaC expression/function.

Dataset Information

Sub-chronic testosterone treatment increases the levels of epithelial sodium channel (ENaC)-?, ? and ? in the kidney of orchidectomized adult male Sprague-Dawley rats.

Publications

Sub-chronic testosterone treatment increases the levels of epithelial sodium channel (ENaC)-α, β and γ in the kidney of orchidectomized adult male Sprague-Dawley rats.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets