Simultaneous Imaging of pH and Peroxynitrite in the Endoplasmic Reticulum and Mitochondria: Revealing Organelle Interactions in Alzheimer’s Disease Pathogenesis

化学 内质网 细胞器 过氧亚硝酸盐 未折叠蛋白反应 发病机制 线粒体 氧化应激 串扰 细胞生物学 生物物理学 生物化学 免疫学 超氧化物 物理 光学 生物
作者
Lushan Huang,Liyi Ma,Qiaowen Zhao,Qianglong Zhu,Guangwei She,Lixuan Mu,Wensheng Shi
出处
期刊:Analytical Chemistry [American Chemical Society]
卷期号:97 (1): 194-202 被引量:8
标识
DOI:10.1021/acs.analchem.4c03646
摘要

pH and peroxynitrite (ONOO-) are two critical biomarkers to unveil the corresponding status of endoplasmic reticulum (ER) stress and mitochondrial dysfunction, which are closely related to Alzheimer's disease (AD). Simultaneously monitoring pH and ONOO- fluctuations in the ER and mitochondria during AD progression is pivotal for clarifying the interplay between the disorders of the two organelles and revealing AD pathogenesis. Herein, we designed and synthesized a dual-channel fluorescent probe (DCFP) to visualize pH and ONOO- in the ER and mitochondria. DCFP possessed excellent sensitivity and selectivity to pH and ONOO- without spectral crosstalk and was utilized in monitoring the two analytes within AD model cells and larval zebrafish. Importantly, DCFP could preferentially target mitochondria in normal cells and be enriched in the ER after mitochondrial depolarization. With the aid of DCFP, the slower acidification rate of the ER than that of mitochondria induced by Aβ oligomers (AβOs) was first identified, which could be ascribed to the relief of the AβOs-triggered ER stress through the Ca2+ migration from the ER to mitochondria. Moreover, continuous exposure to AβOs led to mitochondrial Ca2+ overload, accelerating the acidification and ONOO- overproduction within mitochondria. As a result, intracellular oxidative stress levels were elevated, further exacerbating ER stress and aggravating ER acidification in turn. The advanced understanding of the potential interplay between the ER and mitochondria in this work may offer new insights and methodologies for studying AD pathogenesis. The DCFP developed in this work could also be employed to study other diseases related to ER stress and mitochondrial dysfunction.
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