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Oxygen-dependent regulation of aquaporin-3 expression

Authors Hoogewijs D, Vogler M, Zwenger E, Krull S, Zieseniss A

Received 6 October 2015

Accepted for publication 26 January 2016

Published 21 April 2016 Volume 2016:4 Pages 91—97

DOI https://doi.org/10.2147/HP.S97681

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Thomas Kietzmann

Peer reviewer comments 4

Editor who approved publication: Prof. Dr. Roland Wenger


David Hoogewijs,1,2 Melanie Vogler,3 Eveline Zwenger,3 Sabine Krull,3 Anke Zieseniss3

1Institute of Physiology, University of Duisburg-Essen, Essen, Germany; 2Institute of Physiology, University of Zürich, Zürich, Switzerland; 3Institute of Cardiovascular Physiology, University Medical Center Göttingen, University of Göttingen, Göttingen, Germany

Abstract: The purpose of this study was to investigate whether aquaporin-3 (AQP3) expression is altered in hypoxia and whether hypoxia-inducible transcription factor (HIF)-1 regulates the hypoxic expression. AQP3 mRNA expression was studied in L929 fibrosarcoma cells and in several tissues derived from mice that were subjected to hypoxia. Computational analysis of the AQP3 promoter revealed conserved HIF binding sites within close proximity to the translational start site, and chromatin immunoprecipitation assays confirmed binding of HIF-1 to the endogenous hypoxia response elements. Furthermore, hypoxia resulted in increased expression of AQP3 mRNA in L929 fibrosarcoma cells. Consistently, shRNA-mediated knockdown of HIF-1 greatly reduced the hypoxic induction of AQP3. In addition, mRNA analysis of organs from mice exposed to inspiratory hypoxia demonstrated pronounced hypoxia-inducible expression of AQP3 in the kidney. Overall, our findings suggest that AQP3 expression can be regulated at the transcriptional level and that AQP3 represents a novel HIF-1 target gene.

Keywords: transcriptional regulation, oxygen, hypoxia-inducible factor, hypoxia response element

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