Super-resolution image-based tracking of drug distribution in mitochondria of a label-free naturally derived drug molecules

Wei, Yongchun; Kong, Lingxiu; Chen, Huimin; Liu, Yuanyuan; Xu, Yifei; Wang, Han; Fang, Guiqian; Shao, Xintian; Liu, Fei; Wang, Yanfeng; Chen, Qixin

doi:10.1016/j.cej.2021.132134

Cited by 24 publications

(15 citation statements)

References 58 publications

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“…The apoptosis of macrophages is related to organelles such as mitochondria ( Chen et al, 2020 ; Wang K. et al, 2020 ; Chen et al, 2021 ; Liu et al, 2021a ; Liu et al, 2021b ) ( Figure 1 ). Mitochondria are not only the main sites for intracellular oxidative phosphorylation and the formation of ATP ( Wei et al, 2022 ), but also the sites for the production of ROS ( Forte et al, 2021 ; Wang et al, 2021 ). Oxidation and endoplasmic reticulum (ER) stress can accelerate the apoptosis of macrophages ( Cominacini et al, 2015 ).…”

Section: Opioids Affect the Apoptosis Of Macrophagesmentioning

confidence: 99%

Opioids Regulate the Immune System: Focusing on Macrophages and Their Organelles

et al. 2022

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Opioids are the most widely used analgesics and therefore have often been the focus of pharmacological research. Macrophages are the most plastic cells in the hematopoietic system. They show great functional diversity in various organism tissues and are an important consideration for the study of phagocytosis, cellular immunity, and molecular immunology. The expression of opioid receptors in macrophages indicates that opioid drugs act on macrophages and regulate their functions. This article reviewed the collection of research on effects of opioids on macrophage function. Studies show that opioids, both endogenous and exogenous, can affect the function of macrophages, effecting their proliferation, chemotaxis, transport, phagocytosis, expression of cytokines and chemokine receptors, synthesis and secretion of cytokines, polarization, and apoptosis. Many of these effects are closely associated with mitochondrial function and functions of other organelles in macrophages. Therefore, in depth research into effects of opioids on macrophage organelles may lead to some interesting new discoveries. In view of the important role of macrophages in HIV infection and tumor progression, this review also discusses effects of opioids on macrophages in these two pathological conditions.

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Section: Opioids Affect the Apoptosis Of Macrophagesmentioning

confidence: 99%

Opioids Regulate the Immune System: Focusing on Macrophages and Their Organelles

et al. 2022

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“…To more accurately reflect the damage of 3a to the mitochondria, we applied recently developed structured illumination microscopy (SIM), a new tool for investing the effect of drugs at the single mitochondria level in living cells. ( Wei et al, 2022 ) SIM based on a known spatially structured pattern of light to excite a sample whose fringe position and direction can be changed multiple times and to record the emission fluorescence signal at each position, thereby providing up to 100 nm spatial resolution. ( Chen et al, 2018 ) Therefore, this tool can help us accurately and quantitatively study the behavior of 3a at the nanoscale in living cells system.…”

Section: Resultsmentioning

confidence: 99%

Efficient Synthesis of 2,3′-Spirobi (Indolin)-2′-Ones and Preliminary Evaluation of Their Damage to Mitochondria in HeLa Cells

Sun

et al. 2022

Front. Pharmacol.

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A novel formal (4 + 1) annulation between N-(o-chloromethyl)aryl amides and 3-chlorooxindoles through in situ generated aza-ortho-QMs with 3-chlorooxindoles is reported for the synthesis of a series of 2,3′-spirobi (indolin)-2′-ones in high yields. Under structured illumination microscopy, compound 3a is found to change the mitochondrial morphology and induce mitophagy pathway, which might then trigger mitophagy in cancer cells.

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“…As depicted in Figure 7 , ER Ca 2+ depletion caused by SERCA2b mutations disrupts this balance, leading to the activation of a series of cell-death signaling pathways. Targeted treatments against organelles may be a potential approach to synergistically enhance the neuroprotective function of glutamate receptor inhibitors or glutamate transporters ( Wang K. et al, 2022 ; Wei et al, 2022 ). For example, recovery of the mitochondrial function shows potential therapeutic strategies for traumatic brain injury ( Cheng et al, 2012 ) and neurodegenerative diseases ( Cunnane et al, 2020 ).…”

Section: Discussionmentioning

confidence: 99%

Restoration of Sarco/Endoplasmic Reticulum Ca2+-ATPase Activity Functions as a Pivotal Therapeutic Target of Anti-Glutamate-Induced Excitotoxicity to Attenuate Endoplasmic Reticulum Ca2+ Depletion

Zhang

Pang

et al. 2022

Front. Pharmacol.

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Glutamate-induced excitotoxicity is a pathological basis of many acute/chronic neurodegenerative diseases. Sarco/endoplasmic reticulum Ca2+-ATPase (SERCA2b) is a membrane-embedded P-type ATPase pump that manages the translocation of calcium ions (Ca2+) from cytosol into the lumen of the endoplasmic reticulum (ER) calcium stores. It participates in a wide range of biological functions in the central nervous system (CNS). However, the role of SERCA2b in glutamate-induced excitotoxicity and its mechanism must be elucidated. Herein, we demonstrate that SERCA2b mutants exacerbate the excitotoxicity of hypo-glutamate stimulation on HT22 cells. In this study, SERCA2b mutants accelerated Ca2+ depletion through loss-of-function (reduced pumping capacity) or gain-of-function (acquired leakage), resulting in ER stress. In addition, the occurrence of ER Ca2+ depletion increased mitochondria-associated membrane formation, which led to mitochondrial Ca2+ overload and dysfunction. Moreover, the enhancement of SERCA2b pumping capacity or inhibition of Ca2+ leakage attenuated Ca2+ depletion and impeded excitotoxicity in response to hypo-glutamate stimulation. In conclusion, SERCA2b mutants exacerbate ER Ca2+-depletion-mediated excitotoxicity in glutamate-sensitive HT22 cells. The mechanism of disruption is mainly related to the heterogeneity of SERCA2b mutation sites. Stabilization of SRECA2b function is a critical therapeutic approach against glutamate-induced excitotoxicity. These data will expand understanding of organelle regulatory networks and facilitate the discovery and creation of drugs against excitatory/inhibitory imbalance in the CNS.

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Super-resolution image-based tracking of drug distribution in mitochondria of a label-free naturally derived drug molecules

Cited by 24 publications

References 58 publications

Opioids Regulate the Immune System: Focusing on Macrophages and Their Organelles

Opioids Regulate the Immune System: Focusing on Macrophages and Their Organelles

Efficient Synthesis of 2,3′-Spirobi (Indolin)-2′-Ones and Preliminary Evaluation of Their Damage to Mitochondria in HeLa Cells

Restoration of Sarco/Endoplasmic Reticulum Ca2+-ATPase Activity Functions as a Pivotal Therapeutic Target of Anti-Glutamate-Induced Excitotoxicity to Attenuate Endoplasmic Reticulum Ca2+ Depletion

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