Extremely low frequency pulsed electromagnetic fields cause antioxidative defense mechanisms in human osteoblasts via induction of •O2 − and H2O2

Abstract Recently, we identified a specific extremely low-frequency pulsed electromagnetic field (ELF-PEMF) that supports human osteoblast (hOBs) function in an ERK1/2-dependent manner, suggesting reactive oxygen species (ROS) being key regulators in this process. Thus, this study aimed at investiga...

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Autores principales: Sabrina Ehnert, Anne-Kristin Fentz, Anna Schreiner, Johannes Birk, Benjamin Wilbrand, Patrick Ziegler, Marie K. Reumann, Hongbo Wang, Karsten Falldorf, Andreas K. Nussler
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Publicado: Nature Portfolio 2017
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Acceso en línea:https://doaj.org/article/95c05d50719541a18a7de2d6bf37b9d1
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spelling oai:doaj.org-article:95c05d50719541a18a7de2d6bf37b9d12021-12-02T15:05:44ZExtremely low frequency pulsed electromagnetic fields cause antioxidative defense mechanisms in human osteoblasts via induction of •O2 − and H2O210.1038/s41598-017-14983-92045-2322https://doaj.org/article/95c05d50719541a18a7de2d6bf37b9d12017-11-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-14983-9https://doaj.org/toc/2045-2322Abstract Recently, we identified a specific extremely low-frequency pulsed electromagnetic field (ELF-PEMF) that supports human osteoblast (hOBs) function in an ERK1/2-dependent manner, suggesting reactive oxygen species (ROS) being key regulators in this process. Thus, this study aimed at investigating how ELF-PEMF exposure can modulate hOBs function via ROS. Our results show that single exposure to ELF-PEMF induced ROS production in hOBs, without reducing intracellular glutathione. Repetitive exposure (>3) to ELF-PEMF however reduced ROS-levels, suggesting alterations in the cells antioxidative stress response. The main ROS induced by ELF-PEMF were •O2 − and H2O2, therefore expression/activity of antioxidative enzymes related to these ROS were further investigated. ELF-PEMF exposure induced expression of GPX3, SOD2, CAT and GSR on mRNA, protein and enzyme activity level. Scavenging •O2 − and H2O2 diminished the ELF-PEMF effect on hOBs function (AP activity and mineralization). Challenging the hOBs with low amounts of H2O2 on the other hand improved hOBs function. In summary, our data show that ELF-PEMF treatment favors differentiation of hOBs by producing non-toxic amounts of ROS, which induces antioxidative defense mechanisms in these cells. Thus, ELF-PEMF treatment might represent an interesting adjunct to conventional therapy supporting bone formation under oxidative stress conditions, e.g. during fracture healing.Sabrina EhnertAnne-Kristin FentzAnna SchreinerJohannes BirkBenjamin WilbrandPatrick ZieglerMarie K. ReumannHongbo WangKarsten FalldorfAndreas K. NusslerNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-11 (2017)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Sabrina Ehnert
Anne-Kristin Fentz
Anna Schreiner
Johannes Birk
Benjamin Wilbrand
Patrick Ziegler
Marie K. Reumann
Hongbo Wang
Karsten Falldorf
Andreas K. Nussler
Extremely low frequency pulsed electromagnetic fields cause antioxidative defense mechanisms in human osteoblasts via induction of •O2 − and H2O2
description Abstract Recently, we identified a specific extremely low-frequency pulsed electromagnetic field (ELF-PEMF) that supports human osteoblast (hOBs) function in an ERK1/2-dependent manner, suggesting reactive oxygen species (ROS) being key regulators in this process. Thus, this study aimed at investigating how ELF-PEMF exposure can modulate hOBs function via ROS. Our results show that single exposure to ELF-PEMF induced ROS production in hOBs, without reducing intracellular glutathione. Repetitive exposure (>3) to ELF-PEMF however reduced ROS-levels, suggesting alterations in the cells antioxidative stress response. The main ROS induced by ELF-PEMF were •O2 − and H2O2, therefore expression/activity of antioxidative enzymes related to these ROS were further investigated. ELF-PEMF exposure induced expression of GPX3, SOD2, CAT and GSR on mRNA, protein and enzyme activity level. Scavenging •O2 − and H2O2 diminished the ELF-PEMF effect on hOBs function (AP activity and mineralization). Challenging the hOBs with low amounts of H2O2 on the other hand improved hOBs function. In summary, our data show that ELF-PEMF treatment favors differentiation of hOBs by producing non-toxic amounts of ROS, which induces antioxidative defense mechanisms in these cells. Thus, ELF-PEMF treatment might represent an interesting adjunct to conventional therapy supporting bone formation under oxidative stress conditions, e.g. during fracture healing.
format article
author Sabrina Ehnert
Anne-Kristin Fentz
Anna Schreiner
Johannes Birk
Benjamin Wilbrand
Patrick Ziegler
Marie K. Reumann
Hongbo Wang
Karsten Falldorf
Andreas K. Nussler
author_facet Sabrina Ehnert
Anne-Kristin Fentz
Anna Schreiner
Johannes Birk
Benjamin Wilbrand
Patrick Ziegler
Marie K. Reumann
Hongbo Wang
Karsten Falldorf
Andreas K. Nussler
author_sort Sabrina Ehnert
title Extremely low frequency pulsed electromagnetic fields cause antioxidative defense mechanisms in human osteoblasts via induction of •O2 − and H2O2
title_short Extremely low frequency pulsed electromagnetic fields cause antioxidative defense mechanisms in human osteoblasts via induction of •O2 − and H2O2
title_full Extremely low frequency pulsed electromagnetic fields cause antioxidative defense mechanisms in human osteoblasts via induction of •O2 − and H2O2
title_fullStr Extremely low frequency pulsed electromagnetic fields cause antioxidative defense mechanisms in human osteoblasts via induction of •O2 − and H2O2
title_full_unstemmed Extremely low frequency pulsed electromagnetic fields cause antioxidative defense mechanisms in human osteoblasts via induction of •O2 − and H2O2
title_sort extremely low frequency pulsed electromagnetic fields cause antioxidative defense mechanisms in human osteoblasts via induction of •o2 − and h2o2
publisher Nature Portfolio
publishDate 2017
url https://doaj.org/article/95c05d50719541a18a7de2d6bf37b9d1
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