Meeting details menu

Meeting Authors
Meeting Abstracts
Keynote lectures
Oral communications
Poster presentations
Special symposia
Other

Acta Physiologica Congress

Back

Acta Physiologica 2011; Volume 201, Supplement 682
The 90th Annual Meeting of The German Physiological Society
3/26/2011-3/29/2011
Regensburg, Germany


INVOLVEMENT OF POTASSIUM CHANNELS IN ROS SIGNALLING IN HUMAN GRANULOSA CELLS
Abstract number: P243

*Merz-Lange1 J., Einwang1 D., Mayerhofer1 A., Kunz1,2 L.

Studies in human granulosa cells (hGCs), isolated from follicular aspirates of in vitro-fertilisation (IVF) patients, showed that the A-type K+ current (IA) is predominant in these cells. The presence of Kv4.2 and Kv3.4 in follicles and corpora lutea indicates a physiological role in the human ovary of both, the specific channels and IA itself. The function of this current, which is almost exclusively known in excitable cells, could however not yet be explained in the potentially unexcitable hGCs. In developing follicles specific and changing oxygen and redox-situations exist. While in pig, H2O2 appears to be abundant in follicular fluids, in human IVF-derived follicular fluids, we could neither detect H2O2 in freshly obtained samples nor immediately after addition of various H2O2 concentrations. This points at a highly competent H2O2 degrading system in the human follicle and at a possible role for H2O2 as part of the cellular microenvironment. Addition of H2O2 to cultured hGCs did not raise isoprostan levels, which can be viewed as a measure of lipid-peroxidation and, therefore, cell damage. However, H2O2 robustly induced intracellular reactive oxygen species (ROS), which may act as signalling factors. When combined with specific channel blockers Phrixotoxin-2 and BDS-I, H2O2 generated ROS-levels were significantly lower, showing that blockage of major IA components Kv4.2 and Kv3.4 affects redox state sensing or forwarding. These results imply that IA, which is carried mainly by Kv4.2 and Kv3.4, is a part of a redoxbased signalling system in the human ovary. Supported by DFG KU 1282/5-1

To cite this abstract, please use the following information:
Acta Physiologica 2011; Volume 201, Supplement 682 :P243

Our site uses cookies to improve your experience.You can find out more about our use of cookies in our standard cookie policy, including instructions on how to reject and delete cookies if you wish to do so.

By continuing to browse this site you agree to us using cookies as described in our standard cookie policy .

CLOSE