ArticleJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology2018
Methamphetamine Induces Apoptosis of Microglia via the Intrinsic Mitochondrial-Dependent Pathway.
Article in Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 61 citations in OpenAlex.
- Sigma-1 receptor regulates HIV-1 and methamphetamine-induced endothelial/pericyte barrier impairment via strain-specific inflammatory responses and mitochondrial dysregulation.Journal of neuroinflammation · 2026Article
- The effects of abused drugs on ferroptosis pathways: potential therapeutic targets for substance use disorders.Frontiers in cellular neuroscience · 2026Review
- Selenium and Lycopene Ameliorate Methamphetamine-induced Neurotoxicity in Offspring Rats by Suppressing Oxidative Stress, Neuro-inflammation, and Apoptosis.Biological trace element research · 2026Article
- Neuroprotective Effects of Platelet-Derived Exosomes in a Rat Model of Methamphetamine-Induced Neurotoxicity.Molecular neurobiology · 2025Article
- The interaction between central and peripheral immune systems in methamphetamine use disorder: current status and future directions.Journal of neuroinflammation · 2025Review
- Rotenone and Its Derivative, Rotenoisin A, Induce Neurodegeneration Differentially in SH-SY5Y Cells.Biomedicines · 2024Article
- Neuroprotective activity of green synthesized silver nanoparticles against methamphetamine-induced cell death in human neuroblastoma SH-SY5Y cells.Scientific reports · 2023Article
- Role of Microglia in Psychostimulant Addiction.Current neuropharmacology · 2023Review
- Effects and associated transcriptomic landscape changes of methamphetamine on immune cells.BMC medical genomics · 2022Article
- Methamphetamine Dysregulation of the Central Nervous System and Peripheral Immunity.The Journal of pharmacology and experimental therapeutics · 2021Review
- Neural-Induced Human Adipose Tissue-Derived Stem Cells Conditioned Medium Ameliorates Rotenone-Induced Toxicity in SH-SY5Y Cells.International journal of molecular sciences · 2021Article
- Therapeutic Effects of Conditioned Medium of Neural Differentiated Human Bone Marrow-Derived Stem Cells on Rotenone-Induced Alpha-Synuclein Aggregation and Apoptosis.Stem cells international · 2021Article
- Suicide Attempts and Perceived Social Support among Chinese Drug Users: The Mediating Role of Self-Esteem and Depression.International journal of environmental research and public health · 2020Article
- Methamphetamine alters the TLR4 signaling pathway, NF-κB activation, and pro-inflammatory cytokine production in LPS-challenged NR-9460 microglia-like cells.Molecular immunology · 2020Article
- Comparative phase imaging of live cells by digital holographic microscopy and transport of intensity equation methods.Optics express · 2020Article
- TBHQ-Overview of Multiple Mechanisms against Oxidative Stress for Attenuating Methamphetamine-Induced Neurotoxicity.Oxidative medicine and cellular longevity · 2020Review
- Methamphetamine-induced apoptosis in glial cells examined under marker-free imaging modalities.Journal of biomedical optics · 2019Article
- Methamphetamine Impairs IgG1-Mediated Phagocytosis and Killing of Cryptococcus neoformans by J774.16 Macrophage- and NR-9640 Microglia-Like Cells.Infection and immunity · 2019Article
- Tea Polyphenols Attenuate Methamphetamine-Induced Neuronal Damage in PC12 Cells by Alleviating Oxidative Stress and Promoting DNA Repair.Frontiers in physiology · 2019Article
- Role of C/EBP-β in Methamphetamine-Mediated Microglial Apoptosis.Frontiers in cellular neuroscience · 2019Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Methamphetamine (METH) is a drug of abuse, the acute and chronic use of which induces neurotoxic responses in the human brain, ultimately leading to neurocognitive disorders. Our goals were to understand the impact of METH on microglial mitochondrial respiration and to determine whether METH induces the activation of the mitochondrial-dependent intrinsic apoptosis pathway in microglia. We assessed the expression of pro- apoptosis genes using qPCR of RNA extracted from a human microglial cell line (HTHU). We examined the apoptosis-inducing effects of METH on microglial cells using digital holographic microscopy (DHM) to quantify real-time apoptotic volume decrease (AVD) in microglia in a noninvasive manner. METH treatment significantly increased AVD, activated Caspase 3/7, increased the gene expression levels of the pro- apoptosis proteins, APAF-1 and BAX, and decreased mitochondrial DNA content. Using immunofluorescence analysis, we found that METH increased the expression of the mitochondrial proteins cytochrome c and MCL-1, supporting the activation of mitochondrion-dependent (intrinsic) apoptosis pathway. Cellular bio-energetic flux analysis by Agilent Seahorse XF Analyzer revealed that METH treatment increased both oxidative and glycolytic respiration after 3 h, which was sustained for at least 24 h. Several events, such as oxidative stress, neuro-inflammatory responses, and mitochondrial dysfunction, may converge to mediate METH-induced apoptosis of microglia that may contribute to neurotoxicity of the CNS. Our study has important implications for therapeutic strategies aimed at preserving mitochondrial function in METH abusing patients.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.