17β-Estradiol upregulates distinct maxi-K channel transcripts in mouse uterus

Amanda J. Holdiman, Daniel J. Fergus, Sarah K. England

Research output: Contribution to journalArticle

28 Scopus citations

Abstract

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.

Original languageEnglish
Pages (from-to)1-6
Number of pages6
JournalMolecular and Cellular Endocrinology
Volume192
Issue number1-2
DOIs
StatePublished - Jun 28 2002
Externally publishedYes

Keywords

  • Estrogen
  • Maxi-K channel
  • Mouse
  • Splicing
  • Uterus

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