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Role of plasma dyslipidemia in regulation of macrophage K+ channels: distinct role of oxLDL and acLDL

Our earlier studies have shown that an increase in cellular cholesterol results in suppressing the activity of inwardly‐rectifying K+ (Kir) channels in endothelial cells. Here, we extend these studies to determine the impact of dyslipidemia on Kir channels in macrophages. Our new data show that acLDL and oxLDL have opposite effects on the activity of Kir channels in Bone‐Marrow Derived macrophages (BMDMs). Specifically, we show that loading the cells with cholesterol using either MbCD‐cholesterol complex or acetylated LDL (acLDL) suppressed macrophage Kir‐channel activity but didn't affect Kv‐channels. In contrast, exposure to oxLDL activated both types of channels, an effect opposite to that of acLDL and similar to cholesterol depletion. oxLDL‐induced activation of both Kir and Kv was fully reversed by supplying surplus of cholesterol. Furthermore, we show that monocytes isolated from the bone marrow of dyslipidemic ApoE‐/‐ mice have significantly lower currents than those isolated from the wild type (WT) mice. This effect is observed only immediately after the isolation and is dissipated within 24‐48 hours suggesting that this difference should be attributed to the dyslipidemic environment rather than the loss of ApoE gene per se. Interestingly, an effect of dyslipidemia on resident peritoneal macrophages isolated from ApoE‐/‐ is highly variable with some mice having currents significantly lower than WT controls and some mice showing significantly higher currents. We propose that this variability may be due to variability in the oxidation status of the peritoneal macrophages between mice.