射频波诱导的脂质氧化并通过铁蛋白铁介导导致铁蛋白标记的离子通道的激活。
Lipid Oxidation Induced by RF Waves and Mediated by Ferritin Iron Causes Activation of Ferritin-Tagged Ion Channels.
机构信息
Department of Electrical Engineering and Computer Sciences, University of California, Berkeley, Berkeley, CA 94720, USA; Helen Wills Neuroscience Institute, University of California, Berkeley, Berkeley, CA 94720, USA.
Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA 94720, USA.
出版信息
Cell Rep. 2020 Mar 10;30(10):3250-3260.e7. doi: 10.1016/j.celrep.2020.02.070.
One approach to magnetogenetics uses radiofrequency (RF) waves to activate transient receptor potential channels (TRPV1 and TRPV4) that are coupled to cellular ferritins. The mechanisms underlying this effect are unclear and controversial. Theoretical calculations suggest that the heat produced by RF fields is likely orders of magnitude weaker than needed for channel activation. Using the FeRIC (Ferritin iron Redistribution to Ion Channels) system, we have uncovered a mechanism of activation of ferritin-tagged channels via a biochemical pathway initiated by RF disturbance of ferritin and mediated by ferritin-associated iron. We show that, in cells expressing TRPV channels, RF increases the levels of the labile iron pool in a ferritin-dependent manner. Free iron participates in chemical reactions, producing reactive oxygen species and oxidized lipids that ultimately activate the TRPV channels. This biochemical pathway predicts a similar RF-induced activation of other lipid-sensitive TRP channels and may guide future magnetogenetic designs.
一种磁遗传学方法使用射频 (RF) 波来激活与细胞铁蛋白偶联的瞬时受体电位通道 (TRPV1 和 TRPV4)。这种效应的机制尚不清楚且存在争议。理论计算表明，RF 场产生的热量可能比通道激活所需的量级弱得多。使用 FeRIC（铁蛋白铁重新分配到离子通道）系统，我们发现了一种通过铁蛋白紊乱和铁蛋白相关铁介导的生化途径激活铁蛋白标记通道的机制。我们表明，在表达 TRPV 通道的细胞中，RF 以铁蛋白依赖的方式增加了不稳定铁池的水平。游离铁参与化学反应，产生活性氧和氧化脂质，最终激活 TRPV 通道。这种生化途径预测其他脂质敏感的 TRP 通道也会受到类似的 RF 诱导激活，并且可能为未来的磁遗传学设计提供指导。
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