Zhang W. Epigenetics of epithelial Na+ channel-dependent sodium uptake and blood pressure regulation. World J Nephrol 2015; 4(3): 363-366 [PMID: 26167459 DOI: 10.5527/wjn.v4.i3.363]
Corresponding Author of This Article
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
Research Domain of This Article
Biochemistry & Molecular Biology
Article-Type of This Article
Minireviews
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
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.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
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.
