Epigenetics of epithelial Na+ channel-dependent sodium uptake and blood pressure regulation

doi:10.5527/wjn.v4.i3.363

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World Journal of Nephrology

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2220-6124

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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

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World J Nephrol. Jul 6, 2015; 4(3): 363-366
Published online Jul 6, 2015. doi: 10.5527/wjn.v4.i3.363

Epigenetics of epithelial Na⁺ channel-dependent sodium uptake and blood pressure regulation

Wenzheng Zhang

Wenzheng Zhang, Graduate School of Biomedical Sciences, the University of Texas Health Science Center at Houston, Houston, TX 77030, United States

Wenzheng Zhang, Department of Internal Medicine, University of Texas Medical School at Houston, Houston, TX 77030, United States

Author contributions: The author solely contributed to this paper.

Supported by National Institutes of Health Grant 2R01 DK080236 06A1.

Conflict-of-interest statement: The author has declared that no conflict of interest exists.

Correspondence to: Wenzheng Zhang, Associate Professor, Department of Internal Medicine, University of Texas Medical School at Houston, MSB 5.135, 6431 Fannin, Houston, TX 77030, United States. wenzheng.zhang@uth.tmc.edu

Telephone: +1-713-5006862 Fax: +1-713-5006882

Received: November 1, 2014
Peer-review started: November 9, 2014
First decision: November 27, 2014
Revised: May 6, 2015
Accepted: May 16, 2015
Article in press: May 18, 2015
Published online: July 6, 2015
Processing time: 246 Days and 19.4 Hours

Core Tip

Core tip: The epithelial Na⁺ channel (ENaC) is a key player in sodium transport and blood pressure control. This minireview summarizes the epigenetic mechanisms governing the transcription of αENaC. The epigenetic control involves Dot1a-Af9-mediated repression through targeted hypermethylation of histone H3 K79. Aldosterone relieves the repression by decreasing Dot1a and Af9 mRNA levels and by weakening the protein-protein interaction between Dot1a and Af9 interaction via Sgk1-catalyzed Af9 phosphorylation. Aldosterone-independent mechanism involves Af17 as a competitor of Af9 for binding Dot1a and stimulator of Dot1a nuclear export. Af17^-/- mice exhibit decreased Na⁺ reabsorption and lowered blood pressure, indicating the significance of this epigenetic control.