Key result
Co-expression of KCNE1 slowed activation and suppressed inward rectification of Kv7.5 currents, while KCNE3 drastically inhibited them in Xenopus oocytes and HEK-293 cells.
KCNE1 and KCNE3 functionally interact with Kv7.5 channels to modulate their currents, suggesting a mechanism for fine-tuning cellular responses in skeletal and smooth muscle.
Findings remain preclinical; leaves open whether KCNE subunits regulate Kv7.5 in native human muscle.
Kv7 (KCNQ) proteins form a family of voltage-gated potassium channels that is comprised of five members, Kv7.1-Kv7.5. While Kv7.1 is crucial in the heart, the Kv7.2, Kv7.3, Kv7.4 and Kv7.5 channels contribute to the M-current in the nervous system. In addition to the brain, Kv7.5 is expressed in skeletal and smooth muscle, where its physiological role is currently under evaluation. Kv7 associations with KCNE accessory subunits (KCNE1-5) enhance channel diversity and their interaction provides mechanisms to respond to a variety of stimuli. KCNE peptides control the surface expression, voltage-dependence, kinetics of gating, unitary conductance, ion selectivity and pharmacology of several channels. KCNE subunits have been primarily studied in the heart; however, their activity in the brain and in many other tissues is being increasingly recognized. Here, we found that Kv7.5 and KCNE subunits are present in myoblasts. Therefore, oligomeric associations may underlie some Kv7.5 functional diversity in skeletal muscle. An extensive study in Xenopus oocytes and HEK-293 cells demonstrates that KCNE1 and KCNE3, but none of the other KCNE subunits, affect Kv7.5 currents. While KCNE1 slows activation and suppresses inward rectification, KCNE3 drastically inhibits Kv7.5 currents. In addition, KCNE1 increases Kv7.5 currents in HEK cells. Changes in gating and amplitude indicate functional interactions. Our results have physiological relevance since Kv7.5 is abundant in skeletal and smooth muscle and its association with KCNE peptides may fine-tune cellular responses.
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Roura‐Ferrer et al. (2009) studied this question. KCNE1 and KCNE3 co-expression vs. Kv7.5 alone was evaluated on Kv7.5 currents. Co-expression of KCNE1 slowed activation and suppressed inward rectification of Kv7.5 currents, while KCNE3 drastically inhibited them in Xenopus oocytes and HEK-293 cells.
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