Why the study?
The activity of neuronal Kv7.2/Kv7.3 channels depends on PIP2 and is modulated by cholesterol, but the crosstalk between cholesterol and PIP2 in their regulation remains to be defined.
Cholesterol depletion enhances the interaction between neuronal Kv7.2/Kv7.3 channels and PIP2, reducing their sensitivity to PIP2 dephosphorylation.
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Cholesterol depletion blunts Kv7.2/3 PIP2 sensitivity; leaves open relevance to neuronal or cardiac excitability.
The activity of neuronal Kv7.2/Kv7.3 channels is critically dependent on PIP 2 and finely modulated by cholesterol. Here, we report the crosstalk between cholesterol and PIP 2 in the regulation of Kv7.2/Kv7.3 channels. Our results show that currents passing through Kv7.2/Kv7.3 channels in cholesterol-depleted cells, by acute application of methyl-β-cyclodextrin (MβCD), were less sensitive to PIP 2 dephosphorylation strategies than those of control cells, suggesting that cholesterol depletion enhances the Kv7.2/Kv7.3–PIP 2 interaction. In contrast, the sensitivity of Kv7.2/Kv7.3 channels to acute membrane cholesterol depletion by MβCD was not altered in mutant channels with different apparent affinities for PIP 2 .
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Delgado‐Ramírez et al. (2023) studied this question.
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