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TREK‐1 Currents in Smooth Muscle Cells From Pregnant Human Myometrium
Author(s) -
Heyman Nathanael S,
Barnett Scott,
Wu YiYing,
Singer Cherie,
Leblanc Normand,
Hume Joseph,
Buxton Iain L. O.
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1115.20
Subject(s) - myometrium , arachidonic acid , patch clamp , chemistry , microbiology and biotechnology , smooth muscle , intracellular , myocyte , endocrinology , biophysics , medicine , biology , electrophysiology , biochemistry , uterus , enzyme
Expression of the stretch and arachidonic acid activated two pore K + channel TREK‐1 has recently been described in human myometrium with arachidonic acid promoting relaxation, an effect inhibited by the known TREK‐1 blocker Fluphenazine. The goal of the present study was to examine TREK‐1 currents in human myometrium. Using whole cell voltage clamp on both HEK293 cells over‐expressing human TREK‐1 and pregnant human uterine smooth muscle cells, we demonstrate the presence of K + currents with the following properties previously reported for TREK‐1 channels: insensitivity to TEA + , outward rectification, lack of inactivation, activation by arachidonic acid, activation by intracellular acidification, activation by membrane stretch, and block by Fluphenazine. The role of TREK‐1 in human myometrium is yet to be fully defined, but TREK‐1 currents would be expected to promote uterine quiescence, the maintenance of which is required for pregnancy to proceed to term. Proper regulation or potential dysregulation of TREK‐1 could thus be important in the critical transition of the myometrium from quiescent to laboring tissue leading to both term and pre‐term birth. Supported by March of Dimes Prematurity Initiative Grant 21‐FY10‐176 and NIH HD053028 to ILOB.