ArticleToxicological sciences : an official journal of the Society of Toxicology2015
Caspase-11 plays an essential role in methamphetamine-induced dopaminergic neuron apoptosis.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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24 citing papers in PubMed, 51 citations in OpenAlex.
- Therapeutic targeting of neuroinflammation in methamphetamine use disorder.Future medicinal chemistry · 2025Review
- The Common Denominators of Parkinson's Disease Pathogenesis and Methamphetamine Abuse.Current neuropharmacology · 2024Review
- Coenzyme Q10 reduces expression of apoptotic markers in adult rat nucleus accumbens dopaminergic neurons treated with methamphetamine.Molecular biology reports · 2022Article
- Cannabidiol prevents methamphetamine-induced neurotoxicity by modulating dopamine receptor D1-mediated calcium-dependent phosphorylation of methyl-CpG-binding protein 2.Frontiers in pharmacology · 2022Article
- The Role of HSP90α in Methamphetamine/Hyperthermia-Induced Necroptosis in Rat Striatal Neurons.Frontiers in pharmacology · 2021Article
- An overview of the non-canonical inflammasome.Molecular aspects of medicine · 2020Review
- Effect of Parkin on methamphetamine-induced α-synuclein degradation dysfunction in vitro and in vivo.Brain and behavior · 2020Article
- Activation of Trace Amine-Associated Receptor 1 Stimulates an Antiapoptotic Signal Cascade via Extracellular Signal-Regulated Kinase 1/2.Molecular pharmacology · 2019Article
- The role of chaperone-mediated autophagy in neurotoxicity induced by alpha-synuclein after methamphetamine exposure.Brain and behavior · 2019Article
- Implications of alpha-synuclein nitration at tyrosine 39 in methamphetamine-induced neurotoxicityNeural regeneration research · 2019Article
- Role of C/EBP-β in Methamphetamine-Mediated Microglial Apoptosis.Frontiers in cellular neuroscience · 2019Article
- Untargeted Metabolomic Analysis of Rat Neuroblastoma Cells as a Model System to Study the Biochemical Effects of the Acute Administration of Methamphetamine.Metabolites · 2018Article
- Role of GSK3β/α-synuclein axis in methamphetamine-induced neurotoxicity in PC12 cells.Toxicology research · 2018Article
- METH-Induced Neurotoxicity Is Alleviated by Lactulose Pretreatment Through Suppressing Oxidative Stress and Neuroinflammation in Rat Striatum.Frontiers in neuroscience · 2018Article
- Role of CXCR1 and Interleukin-8 in Methamphetamine-Induced Neuronal Apoptosis.Frontiers in cellular neuroscience · 2018Article
- SUMOylation of Alpha-Synuclein Influences on Alpha-Synuclein Aggregation Induced by Methamphetamine.Frontiers in cellular neuroscience · 2018Article
- Molecular pathology of cerebral TNF-α, IL-1β, iNOS and Nrf2 in forensic autopsy cases with special regard to deaths due to environmental hazards and intoxication.Forensic science, medicine, and pathology · 2017Article
- Effects of DDIT4 in Methamphetamine-Induced Autophagy and Apoptosis in Dopaminergic Neurons.Molecular neurobiology · 2017Article
- Nupr1 Modulates Methamphetamine-Induced Dopaminergic Neuronal Apoptosis and Autophagy through CHOP-Trib3-Mediated Endoplasmic Reticulum Stress Signaling Pathway.Frontiers in molecular neuroscience · 2017Article
- Mitochondrial Ferritin Deletion ExacerbatesOxidative medicine and cellular longevity · 2017Article
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Methamphetamine (METH) is an extremely addictive stimulant drug that is widely used with high potential of abuse. Previous studies have shown that METH exposure damages the nervous system, especially dopaminergic neurons. However, the exact molecular mechanisms of METH-induced neurotoxicity remain unclear. We hypothesized that caspase-11 is involved in METH-induced neuronal apoptosis. We tested our hypothesis by examining the change of caspase-11 protein expression in dopaminergic neurons (PC12 and SH-SY5Y) and in the midbrain of rats exposed to METH with Western blotting. We also determined the effects of blocking caspase-11 expression with wedelolactone (a specific inhibitor of caspase-11) or siRNA on METH-induced apoptosis in PC12 cells and SH-SY5Y cells using Annexin V and TUNEL staining. Furthermore, we observed the protein expression changes of the apoptotic markers, cleaved caspase-3 and cleaved poly(ADP-ribose) polymerase 1 (PARP), after silencing the caspase-11 expression in rat midbrain by injecting LV-shcasp11 lentivirus using a stereotaxic positioning system. Results showed that METH exposure increased caspase-11 expression both in vitro and in vivo, with the effects in vitro being dose- and time-dependent. Inhibition of caspase-11 expression with either wedelolactone or siRNAs reduced the number of METH-induced apoptotic cells. In addition, blocking caspase-11 expression inhibited METH-induced activation of caspase-3 and PARP in vitro and in vivo, suggesting that caspase-11/caspase-3 signal pathway is involved in METH-induced neurotoxicity. These results indicate that caspase-11 plays an essential role in METH-induced neuronal apoptosis and may be a potential gene target for therapeutics in METH-caused neurotoxicity.
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