TU Darmstadt / ULB / TUbiblio

X-ray irradiation activates K(+) channels via H2O2 signaling.

Gibhardt, Christine S. and Roth, Bastian and Schroeder, Indra and Fuck, Sebastian and Becker, Patrick and Jakob, Burkhard and Fournier, Claudia and Moroni, Anna and Thiel, Gerhard (2015):
X-ray irradiation activates K(+) channels via H2O2 signaling.
In: Scientific reports, p. 13861, 5, ISSN 2045-2322,
[Article]

Abstract

Ionizing radiation is a universal tool in tumor therapy but may also cause secondary cancers or cell invasiveness. These negative side effects could be causally related to the human-intermediate-conductance Ca(2+)-activated-K(+)-channel (hIK), which is activated by X-ray irradiation and affects cell proliferation and migration. To analyze the signaling cascade downstream of ionizing radiation we use genetically encoded reporters for H2O2 (HyPer) and for the dominant redox-buffer glutathione (Grx1-roGFP2) to monitor with high spatial and temporal resolution, radiation-triggered excursions of H2O2 in A549 and HEK293 cells. The data show that challenging cells with ≥1 Gy X-rays or with UV-A laser micro-irradiation causes a rapid rise of H2O2 in the nucleus and in the cytosol. This rise, which is determined by the rate of H2O2 production and glutathione-buffering, is sufficient for triggering a signaling cascade that involves an elevation of cytosolic Ca(2+) and eventually an activation of hIK channels.

Item Type: Article
Erschienen: 2015
Creators: Gibhardt, Christine S. and Roth, Bastian and Schroeder, Indra and Fuck, Sebastian and Becker, Patrick and Jakob, Burkhard and Fournier, Claudia and Moroni, Anna and Thiel, Gerhard
Title: X-ray irradiation activates K(+) channels via H2O2 signaling.
Language: English
Abstract:

Ionizing radiation is a universal tool in tumor therapy but may also cause secondary cancers or cell invasiveness. These negative side effects could be causally related to the human-intermediate-conductance Ca(2+)-activated-K(+)-channel (hIK), which is activated by X-ray irradiation and affects cell proliferation and migration. To analyze the signaling cascade downstream of ionizing radiation we use genetically encoded reporters for H2O2 (HyPer) and for the dominant redox-buffer glutathione (Grx1-roGFP2) to monitor with high spatial and temporal resolution, radiation-triggered excursions of H2O2 in A549 and HEK293 cells. The data show that challenging cells with ≥1 Gy X-rays or with UV-A laser micro-irradiation causes a rapid rise of H2O2 in the nucleus and in the cytosol. This rise, which is determined by the rate of H2O2 production and glutathione-buffering, is sufficient for triggering a signaling cascade that involves an elevation of cytosolic Ca(2+) and eventually an activation of hIK channels.

Journal or Publication Title: Scientific reports
Volume: 5
Divisions: 10 Department of Biology
10 Department of Biology > Plant Membrane Biophysics
Date Deposited: 16 Sep 2015 11:33
Export:
Suche nach Titel in: TUfind oder in Google

Optionen (nur für Redakteure)

View Item View Item