Transit of H2O2 across the endoplasmic reticulum membrane is not sluggish.

Francisco Laurindo, Ivo P Touw, Michel B Toledano, Roberto Sitia, Thomas Simmen, Michael Rützler, Jan Riemer, Andreas J Meyer, Eva Margittai, Christian Appenzeller-Herzog, Thomas Kietzmann, Agnes Görlach, Henry Jay Forman, Agnès Delaunay-Moisan, Kelvin J A Davies, Ivan Bogeski, Gabor Bánhegyi

Journal: Free radical biology & medicine 2017;94():157-60

PMID: 26928585

Abstract

Cellular metabolism provides various sources of hydrogen peroxide (H2O2) in different organelles and compartments. The suitability of H2O2 as an intracellular signaling molecule therefore also depends on its ability to pass cellular membranes. The propensity of the membranous boundary of the endoplasmic reticulum (ER) to let pass H2O2 has been discussed controversially. In this essay, we challenge the recent proposal that the ER membrane constitutes a simple barrier for H2O2 diffusion and support earlier data showing that (i) ample H2O2 permeability of the ER membrane is a prerequisite for signal transduction, (ii) aquaporin channels are crucially involved in the facilitation of H2O2 permeation, and (iii) a proper experimental framework not prone to artifacts is necessary to further unravel the role of H2O2 permeation in signal transduction and organelle biology.

Copyright © 2016 Elsevier Inc. All rights reserved.

Address: Berufsfachschule Gesundheit Baselland, 4142 Münchenstein, Switzerland. Electronic address: [email protected].; Department of Medical Chemistry, Molecular Biology and Pathobiochemistry, Semmelweis University, Budapest 1428, Hungary.; Department of Biophysics, School of Medicine, University of Saarland, 66421 Homburg, Germany.; Leonard Davis School of Gerontology of the Ethel Percy Andrus Gerontology Center; and Division of Molecular and Computational Biology, Department of Biological Sciences of the Dornsife College of Letters, Arts, and Sciences, The University of Southern California, Los Angeles, CA 90089-0191, USA; Division of Molecular and Computational Biology, Department of Biological Sciences, Dornsife College of Letters, Arts, and Sciences, The University of Southern California, Los Angeles, CA 90089-0191, USA.; Laboratoire Stress Oxydant et Cancers, CEA-Saclay, Institute for Integrative Biology of the Cell (I2BC), 91198 Gif sur Yvette Cedex, France.; Leonard Davis School of Gerontology of the Ethel Percy Andrus Gerontology Center; and Division of Molecular and Computational Biology, Department of Biological Sciences of the Dornsife College of Letters, Arts, and Sciences, The University of Southern California, Los Angeles, CA 90089-0191, USA.; Experimental and Molecular Pediatric Cardiology, German Heart Center Munich at the TU Munich, 80636 Munich, Germany.; Faculty of Biochemistry and Molecular Medicine, University of Oulu, 90210 Oulu, Finland.; Vascular Biology Laboratory, Heart Institute, University of São Paulo School of Medicine, CEP 05403-000 São Paulo, Brazil.; Institute of Human Physiology and Clinical Experimental Research, Semmelweis University, Budapest 1428, Hungary.; INRES-Chemical Signalling, University of Bonn, 53113 Bonn, Germany.; Institute for Biochemistry, University of Cologne, 50674 Cologne, Germany.; Institute for Health Science and Technology, Aalborg University, DK-9220 Aalborg, Denmark.; Department of Cell Biology, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Alberta, Canada T6G2H7.; Protein Transport and Secretion Unit, Division of Genetics and Cell Biology, IRCCS, Ospedale San Raffaele/Universita' Vita-Salute San Raffaele, 20132 Milan, Italy.; Erasmus University Medical Center, Department of Hematology, PO Box 2040, Rotterdam, The Netherlands.

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