The mouse maxi-K channel transcript undergoes alternative splicing to produce isoforms differing in sensitivity to intracellular regulators. We hypothesized that 17β-estradiol could induce myometrial maxi-K channel transcripts to differentially splice. Polymerase chain reaction demonstrated two products at site D in mice injected with either 8.5 μg of 17β-estradiol for 4 days or a vehicle control. Splicing of site D is known to modulate the sensitivity of the maxi-K channel to calcium and voltage. RNase protection analyses revealed that the α subunit transcript, and an exon encoding 59 amino acids at site D that enhances Ca2+- and voltage-sensitivity, are upregulated ∼1.4-fold after 17β-estradiol stimulation however, the insertless isoform of this transcript is enhanced ∼5-fold. Immunoblotting demonstrates that the total maxi-K channel α subunit expression mimics transcript regulation. These findings verify that maxi-K channel transcripts are differentially spliced by 17β-estradiol, which may contribute to stoichiometric changes in isoform expression during pregnancy.
- Maxi-K channel