Altered trafficking of Large Conductance Ca2+‐activated K+ (MaxiK) channels in mouse myometrium during late pregnancy

We have previously demonstrated an overall increase in MaxiK mRNA and protein levels from late‐pregnant (LP) mice myometrium, while channel current density and surface expression is diminished as compared to non‐pregnant (NP) mice. These observations indicate that the reduction in surface expression is due to an altered trafficking of the channels to the cell surface. We hypothesize that MaxiK surface expression is influenced by hormonal changes during pregnancy and that a retention mechanism at the sarcoplasmic reticulum (SR) or the Golgi apparatus is part of the remodeling that occurs before parturition. Here, the subcellular localization of MaxiK in isolated myometrium cells from NP, LP, during parturition (DP) and 24 hours post‐partum (PP) mice are analyzed by confocal microscopy. In NP mice MaxiK channels are primarily localized to the plasma membrane, while in LP mice MaxiK was barely detected at the plasma membrane and was highly concentrated in perinuclear regions significantly overlapping with the SR labeling. Interestingly, 24 hours after parturition MaxiK labeling was absent from the SR and was detected in clusters at the surface membrane as in NP mice. Our results indicate that during late pregnancy the myometrium undergoes remodeling prior to delivery and MaxiK channel expression is significantly reduced at the plasma membrane and sequestered to the SR. MaxiK rapid plasma membrane restoration after pregnancy suggests that the altered trafficking signals might be induced by the expression of pregnancy‐related hormones.