Voltage-dependent K super(+) channel acts as sex steroid sensor in endocrine cells of the human ovary

• Published in: Journal of cellular physiology 2006-01, Vol.206 (1), p.167-174
• Main Authors: Kunz, Lars, Raemsch, Romi, Krieger, Annette, Young, Kelly A, Dissen, Gregory A, Stouffer, Richard L, Ojeda, Sergio R, Mayerhofer, Artur
• Format: Article
• Language: English
• Subjects: Macaca mulatta
• ISSN: 0021-9541; 1097-4652
• DOI: 10.1002/jcp.20453

Molecular targets of rapid non-genomic steroid actions are not well known compared to those of the classical transcription pathway, but ion channels have recently been identified to be steroid-sensitive. Especially, in the ovary, the very organ producing high amounts of sex steroids, their rapid actions are not well examined. We now identified a yet unknown target for sex steroids, a voltage-dependent K super(+) channel (K sub(v)4.2) that contributes to a transient outward K super(+) current (I sub(A)) in human granulosa cells (GCs). Sex steroid hormones at concentrations typical for the ovary (1 mu M) blocked K sub(v)4.2 thereby attenuating I sub(A) by about 25% within seconds. We also found both K sub(v)4.2 (KCND2) mRNA and protein in endocrine cells of the human and rhesus macaque ovary, emphasizing the physiological relevance of this channel. Therefore, we propose a role as fast-responding steroid sensor for the K sub(v)4.2 channel. The direct regulation of K super(+) channel activity by sex steroids might represent a yet unknown mechanism of rapid steroid action in close proximity to the site of steroid production in the primate ovary. Our data might also be important for K sub(v)4 channels in the brain and the cardiovascular system where rapid steroid effects are discussed in the context of prevention of cell death. copyright 2005 Wiley-Liss, Inc.