Purchase this article with an account.
M. Takahira, M. Sakurai, N. Sakurada, K. Sugiyama; Two–Pore Domain K+ Channel Expressed in the Human Corneal Epithelium . Invest. Ophthalmol. Vis. Sci. 2006;47(13):67.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
The large conductance K+ channel in the corneal epithelium maintains cell homeostasis and may regulate migration and differentiation of the corneal epithelium. Its pharmacological and electrophysiological properties indicate that the candidate origin is a two–pore domain K+ channel, TREK (tandem of pore domains in a weak inward rectifying K+ channel–related K+ channel). The purpose of this study was to investigate expression of TREK channel in the human corneal epithelium.
Human corneal epithelial cells (HCEC, Kurabo Industries, Osaka Japan) were cultured in EpiLife® Medium with Human Corneal Growth Supplement (Kurabo Industries). HCEC were enzymatically dissociated and purfused with HEPES–buffered Ringer solutions. Whole–cell currents in HCEC were recorded using the patch–clamp technique. TREK mRNA expression in HCEC was examined using RT–PCR.
The zero–current potential in HCEC bathed with the standard Ringer solution averaged –13 mV (n = 84). Outwardly rectifying, noisy currents dominated the whole cell current in HCEC. This current component was markedly stimulated by external application of 100 µM flufenamic acid, 20 µM arachidonic acid, and 100 µM palmitoleic acid with the reversal potentials near the equilibrium potential for K+. The augmented K+ current was inhibited almost completely by 100 µM diltiazem. mRNAs of TREK–1 and TREK–2 were detected in HCEC. The amount of TREK–2 mRNA was obviously predominant over TREK–1 mRNA.
The large conductance K+ channel is expressed in the human corneal epithelial cells. The candidate origin for this channel is a 2P domain K+ channel subfamily, TREK.
This PDF is available to Subscribers Only