Transit of H2O2 across the endoplasmic reticulum membrane is not sluggish

被引：42

作者：

Appenzeller-Herzog, Christian ^{[1
]}

Banhegyi, Gabor ^{[2
]}

Bogeski, Ivan ^{[3
]}

Davies, Kelvin J. A. ^{[4
,5
]}

Delaunay-Moisan, Agnes ^{[6
]}

Forman, Henry Jay ^{[4
,5
]}

Goerlach, Agnes ^{[7
]}

Kietzmann, Thomas ^{[8
]}

Laurindo, Francisco ^{[9
]}

Margittai, Eva ^{[10
]}

Meyer, Andreas J. ^{[11
]}

Riemer, Jan ^{[12
]}

Rutzler, Michael ^{[13
]}

Simmen, Thomas ^{[14
]}

Sitia, Roberto ^{[15
]}

Toledano, Michel B. ^{[6
]}

Touw, Ivo P. ^{[16
]}

机构：

[1] Berufsfachschule Gesundheit Baselland, CH-4142 Munchenstein, Switzerland

[2] Semmelweis Univ, Dept Med Chem Mol Biol & Pathobiochem, H-1428 Budapest, Hungary

[3] Univ Saarland, Sch Med, Dept Biophys, D-66421 Homburg, Germany

[4] Univ So Calif, Ethel Percy Andrus Gerontol Ctr, Leonard Davis Sch Gerontol, Los Angeles, CA 90089 USA

[5] Univ So Calif, Dornsife Coll Letters Arts & Sci, Dept Biol Sci, Div Mol & Computat Biol, Los Angeles, CA 90089 USA

[6] CEA Saclay, Lab Stress Oxydant & Canc, I2BC, F-91198 Gif Sur Yvette, France

[7] Tech Univ Munich, German Heart Ctr Munich, Expt & Mol Pediat Cardiol, D-80636 Munich, Germany

[8] Univ Oulu, Fac Biochem & Mol Med, Oulu 90210, Finland

[9] Univ Sao Paulo, Sch Med, Inst Heart, Vasc Biol Lab, BR-05403000 Sao Paulo, Brazil

[10] Semmelweis Univ, Inst Human Physiol & Clin Expt Res, H-1428 Budapest, Hungary

[11] Univ Bonn, INRES Chem Signalling, D-53113 Bonn, Germany

[12] Univ Cologne, Inst Biochem, D-50674 Cologne, Germany

[13] Aalborg Univ, Inst Hlth Sci & Technol, DK-9220 Aalborg, Denmark

[14] Univ Alberta, Fac Med & Dent, Dept Cell Biol, Edmonton, AB T6G 2H7, Canada

[15] Univ Vita Salute San Raffaele, Osped San Raffaele, IRCCS, Prot Transport & Secret Unit,Div Genet & Cell Bio, I-20132 Milan, Italy

[16] Erasmus Univ, Med Ctr, Dept Hematol, POB 2040, Rotterdam, Netherlands

来源：

FREE RADICAL BIOLOGY AND MEDICINE | 2016年 / 94卷

关键词：

PROTEIN-TYROSINE PHOSPHATASES; AQUAPORIN-11 KNOCKOUT MICE; GLUTATHIONE-PEROXIDASE; 7; HYDROGEN-PEROXIDE; DNA-DAMAGE; REDOX REGULATION; NOX4; RECEPTOR; INACTIVATION; VACUOLIZATION;

D O I：

10.1016/j.freeradbiomed.2016.02.030

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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. (C) 2016 Elsevier Inc. All rights reserved.

引用

页码：157 / 160

页数：4

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