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使用生物传感器测定内质网中烟碱类药物的药代动力学。

Determining the pharmacokinetics of nicotinic drugs in the endoplasmic reticulum using biosensors.

机构信息

Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, CA.

Janelia Research Campus, Howard Hughes Medical Institute, Ashburn, VA.

出版信息

J Gen Physiol. 2019 Jun 3;151(6):738-757. doi: 10.1085/jgp.201812201. Epub 2019 Feb 4.

Abstract

Nicotine dependence is thought to arise in part because nicotine permeates into the endoplasmic reticulum (ER), where it binds to nicotinic receptors (nAChRs) and begins an "inside-out" pathway that leads to up-regulation of nAChRs on the plasma membrane. However, the dynamics of nicotine entry into the ER are unquantified. Here, we develop a family of genetically encoded fluorescent biosensors for nicotine, termed iNicSnFRs. The iNicSnFRs are fusions between two proteins: a circularly permutated GFP and a periplasmic choline-/betaine-binding protein engineered to bind nicotine. The biosensors iNicSnFR3a and iNicSnFR3b respond to nicotine by increasing fluorescence at [nicotine] <1 µM, the concentration in the plasma and cerebrospinal fluid of a smoker. We target iNicSnFR3 biosensors either to the plasma membrane or to the ER and measure nicotine kinetics in HeLa, SH-SY5Y, N2a, and HEK293 cell lines, as well as mouse hippocampal neurons and human stem cell-derived dopaminergic neurons. In all cell types, we find that nicotine equilibrates in the ER within 10 s (possibly within 1 s) of extracellular application and leaves as rapidly after removal from the extracellular solution. The [nicotine] in the ER is within twofold of the extracellular value. We use these data to run combined pharmacokinetic and pharmacodynamic simulations of human smoking. In the ER, the inside-out pathway begins when nicotine becomes a stabilizing pharmacological chaperone for some nAChR subtypes, even at concentrations as low as ∼10 nM. Such concentrations would persist during the 12 h of a typical smoker's day, continually activating the inside-out pathway by >75%. Reducing nicotine intake by 10-fold decreases activation to ∼20%. iNicSnFR3a and iNicSnFR3b also sense the smoking cessation drug varenicline, revealing that varenicline also permeates into the ER within seconds. Our iNicSnFRs enable optical subcellular pharmacokinetics for nicotine and varenicline during an early event in the inside-out pathway.

摘要

尼古丁依赖被认为部分是由于尼古丁渗透到内质网 (ER) 中,在那里它与烟碱型乙酰胆碱受体 (nAChR) 结合,并开始一种“内向外”途径,导致质膜上 nAChR 的上调。然而,尼古丁进入 ER 的动力学尚未量化。在这里,我们开发了一系列用于尼古丁的基因编码荧光生物传感器,称为 iNicSnFRs。iNicSnFRs 是两种蛋白质的融合:一种是经过环状排列的 GFP 和一种经过工程改造以结合尼古丁的周质胆碱/甜菜碱结合蛋白。生物传感器 iNicSnFR3a 和 iNicSnFR3b 在 [尼古丁] <1µM 时通过增加荧光来响应尼古丁,这是吸烟者血浆和脑脊液中的浓度。我们将 iNicSnFR3 生物传感器靶向质膜或内质网,并在 HeLa、SH-SY5Y、N2a 和 HEK293 细胞系以及小鼠海马神经元和人干细胞衍生的多巴胺能神经元中测量尼古丁动力学。在所有细胞类型中,我们发现尼古丁在细胞外应用后 10 秒内(可能在 1 秒内)在 ER 中达到平衡,并在从细胞外溶液中去除后迅速离开。ER 中的 [尼古丁] 与细胞外值相差两倍。我们使用这些数据对人类吸烟的药代动力学和药效动力学进行联合模拟。在内质网中,当尼古丁成为某些 nAChR 亚型的稳定药理学伴侣时,即使在低至约 10 nM 的浓度下,也会开始“内向外”途径。在典型吸烟者一天的 12 小时内,这种浓度会持续存在,通过 >75%持续激活“内向外”途径。将尼古丁摄入量减少 10 倍会将激活作用降低到约 20%。iNicSnFR3a 和 iNicSnFR3b 还能感知戒烟药物伐伦克林,表明伐伦克林也能在数秒内渗透到内质网中。我们的 iNicSnFRs 使尼古丁和伐伦克林在“内向外”途径的早期事件中进行光学亚细胞药代动力学研究成为可能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd4d/6571994/1dd22198e332/JGP_201812201_GA.jpg

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