Laboratory of Ion Channel Research, Department of Cellular and Molecular Medicine, KU Leuven, 3000 Leuven, Belgium.
VIB Center for Brain & Disease Research, 3000 Leuven, Belgium.
Int J Mol Sci. 2021 Mar 25;22(7):3368. doi: 10.3390/ijms22073368.
The Transient Receptor Potential Ankyrin 1 cation channel (TRPA1) is a broadly-tuned chemosensor expressed in nociceptive neurons. Multiple TRPA1 agonists are chemically unrelated non-electrophilic compounds, for which the mechanisms of channel activation remain unknown. Here, we assess the hypothesis that such chemicals activate TRPA1 by inducing mechanical perturbations in the plasma membrane. We characterized the activation of mouse TRPA1 by non-electrophilic alkylphenols (APs) of different carbon chain lengths in the para position of the aromatic ring. Having discarded oxidative stress and the action of electrophilic mediators as activation mechanisms, we determined whether APs induce mechanical perturbations in the plasma membrane using dyes whose fluorescence properties change upon alteration of the lipid environment. APs activated TRPA1, with potency increasing with their lipophilicity. APs increased the generalized polarization of Laurdan fluorescence and the anisotropy of the fluorescence of 1,6-diphenyl-1,3,5-hexatriene (DPH), also according to their lipophilicity. Thus, the potency of APs for TRPA1 activation is an increasing function of their ability to induce lipid order and membrane rigidity. These results support the hypothesis that TRPA1 senses non-electrophilic compounds by detecting the mechanical alterations they produce in the plasma membrane. This may explain how structurally unrelated non-reactive compounds induce TRPA1 activation and support the role of TRPA1 as an unspecific sensor of potentially noxious compounds.
瞬时受体电位锚蛋白 1 阳离子通道(TRPA1)是一种广泛调节的化学感受器,表达于伤害感受神经元中。多种 TRPA1 激动剂在化学上是无电活性的非亲电子化合物,其通道激活的机制尚不清楚。在这里,我们评估了这样一种假说,即这些化学物质通过在质膜中引起机械扰动来激活 TRPA1。我们在芳香环对位上具有不同碳链长度的非电活性烷基酚(APs)的情况下,表征了小鼠 TRPA1 的激活。在排除了氧化应激和亲电子介质的作用作为激活机制之后,我们使用其荧光性质在脂质环境改变时发生变化的染料来确定 APs 是否在质膜中引起机械扰动。APs 激活了 TRPA1,其效力随疏水性的增加而增加。APs 增加了 Laurdan 荧光的广义极化和 1,6-二苯基-1,3,5-己三烯(DPH)的荧光各向异性,这也与它们的疏水性有关。因此,APs 对 TRPA1 激活的效力是其诱导脂质有序性和膜刚性的能力的递增函数。这些结果支持了这样一种假说,即 TRPA1 通过检测它们在质膜中产生的机械变化来感知非电活性化合物。这可以解释为什么结构上不相关的非反应性化合物会诱导 TRPA1 的激活,并支持 TRPA1 作为潜在有害化合物的非特异性传感器的作用。