17β-Estradiol Inhibits Outward Voltage-Gated K+ Currents in Human Osteoblast-Like MG63 Cells
Previous studies have shown that 17β-estradiol has a pivotal function by blocking voltage-gated K + (Kv) channels in several different types of cells such as cardiac myocytes and neurons. Outward Kv currents can also be measured in osteoblasts, although little is known about the effects of 17β-estra...
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Published in | The Journal of membrane biology Vol. 246; no. 1; pp. 39 - 45 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
New York
Springer-Verlag
2013
|
Subjects | |
Online Access | Get full text |
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Summary: | Previous studies have shown that 17β-estradiol has a pivotal function by blocking voltage-gated K
+
(Kv) channels in several different types of cells such as cardiac myocytes and neurons. Outward Kv currents can also be measured in osteoblasts, although little is known about the effects of 17β-estradiol on these currents. In human osteoblast-like MG63 cells, we found that 17β-estradiol inhibits peak and end Kv currents, with IC
50
values of 480 and 325 nM, respectively. To elucidate the mechanism of inhibition, the kinetics of Kv currents were investigated. The half-maximum activation potential (
V
1/2
) was 1.3 mV and was shifted left to −4.4 mV after application of 500 nM 17β-estradiol. For steady-state inactivation, the
V
1/2
was –55.0 mV and weakly shifted left to –58.2 mV. To identify the molecular basis of outward Kv currents in MG63 cells, we performed RT-PCR analyses. The expression of Kv2.1 channels appeared to dominate over that of other Kv channels in MG63 cells. In COS-7 cells with heterologously expressed Kv2.1 channels, 17β-estradiol also inhibits macroscopic currents of Kv2.1. Our data indicate that 17β-estradiol inhibits Kv currents in human osteoblast-like MG63 cells and that Kv2.1 is a potential molecular correlate of outward Kv currents in these cells. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0022-2631 1432-1424 |
DOI: | 10.1007/s00232-012-9502-y |