Methamphetamine induces GSDME-dependent cell death in hippocampal neuronal cells through the endoplasmic reticulum stress pathway

Liu, Yi; Wen, Di; Gao, Jingqi; Xie, Bing; Yu, Hailei; Shen, Qianchao; Zhang, Jingjing; Jing, W; Cong, Bin; Ma, Chunling

doi:10.1016/j.brainresbull.2020.06.005

Cited by 19 publications

(14 citation statements)

References 63 publications

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“…These phenomena were attenuated by aspirin-triggered-lipoxin A4 (ATL), a potent anti-inflammatory mediator [ 115 ]. In various cells, including cardiomyocytes, microglia, and neurons, METH induces apoptosis and pyroptosis through the NLRP-Caspase1-GSDMD pathway [ 116 ]. Therefore, METH exposures increased NLRP1 and NLRP3 inflammasome levels as well as neuroinflammation responses in the brain, followed by neurotoxicity and substantial damage to the brain.…”

Section: Roles Of Nlrp Inflammasome In Neuropsychiatric Disordersmentioning

confidence: 99%

The Significance of NLRP Inflammasome in Neuropsychiatric Disorders

et al. 2022

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The NLRP inflammasome is a multi-protein complex which mainly consists of the nucleotide-binding oligomerization domain, leucine-rich repeat, and pyrin domain. Its activation is linked to microglial-mediated neuroinflammation and partial neuronal degeneration. Many neuropsychiatric illnesses have increased inflammatory responses as both a primary cause and a defining feature. The NLRP inflammasome inhibition delays the progression and alleviates the deteriorating effects of neuroinflammation on several neuropsychiatric disorders. Evidence on the central effects of the NLRP inflammasome potentially provides the scientific base of a promising drug target for the treatment of neuropsychiatric disorders. This review elucidates the classification, composition, and functions of the NLRP inflammasomes. It also explores the underlying mechanisms of NLRP inflammasome activation and its divergent role in neuropsychiatric disorders, including Alzheimer’s disease, Huntington’s disease, Parkinson’s disease, depression, drug use disorders, and anxiety. Furthermore, we explore the treatment potential of the NLRP inflammasome inhibitors against these disorders.

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Section: Roles Of Nlrp Inflammasome In Neuropsychiatric Disordersmentioning

confidence: 99%

The Significance of NLRP Inflammasome in Neuropsychiatric Disorders

et al. 2022

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“…It has also been observed that toxic doses of methamphetamine significantly increase the expression of PERK and caspase-12 and that these effects can be diminished by inhibiting cyclin-dependent kinase 5(CDK5), an enzyme t phosphorylates Tau ( Hashiguchi et al, 2002 ). Moreover, Liu et al ( Liu et al, 2020 ) found that METH signaled through three ER stress pathways in hippocampal neuronal cells (HT-22) in a time- and dose-dependent manner. The disruption of ER functions induced by METH is accompanied by altered ER calcium homeostasis ( Chen et al, 2019 ).…”

Section: Pcd Signaling Pathways and Their Roles In Meth-induced Neuro...mentioning

confidence: 99%

Molecular mechanisms of programmed cell death in methamphetamine-induced neuronal damage

et al. 2022

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Methamphetamine, commonly referred to as METH, is a highly addictive psychostimulant and one of the most commonly misused drugs on the planet. Using METH continuously can increase your risk for drug addiction, along with other health complications like attention deficit disorder, memory loss, and cognitive decline. Neurotoxicity caused by METH is thought to play a significant role in the onset of these neurological complications. The molecular mechanisms responsible for METH-caused neuronal damage are discussed in this review. According to our analysis, METH is closely associated with programmed cell death (PCD) in the process that causes neuronal impairment, such as apoptosis, autophagy, necroptosis, pyroptosis, and ferroptosis. In reviewing this article, some insights are gained into how METH addiction is accompanied by cell death and may help to identify potential therapeutic targets for the neurological impairment caused by METH abuse.

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“…In this study, METH combined with HT triggered necroptosis in striatal neurons after 6 h. The inhibition of HSP90α decreased the METH/HT-induced upregulation of p-RIP3, RIP3, p-MLKL, and MLKL, suggesting that HSP90α may mediate necroptosis by regulating the phosphorylation of RIP3. Interestingly, pyroptosis, an inflammasome-associated regulatory necrosis, is closely associated with the pathogenesis of neurodegenerative diseases ( Wang et al, 2019 ; Huang et al, 2021 ) and METH induces ER stress that mediates GSDME-dependent pyroptosis in hippocampal neuronal cells ( Liu et al, 2020 ). That is to say, METH abuse may cause a variety of regulatory cell necrosis.…”

Section: Discussionmentioning

confidence: 99%

The Role of HSP90α in Methamphetamine/Hyperthermia-Induced Necroptosis in Rat Striatal Neurons

Liao

Yan

et al. 2021

Front. Pharmacol.

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Methamphetamine (METH) is one of the most widely abused synthetic drugs in the world. The users generally present hyperthermia (HT) and psychiatric symptoms. However, the mechanisms involved in METH/HT-induced neurotoxicity remain elusive. Here, we investigated the role of heat shock protein 90 alpha (HSP90α) in METH/HT (39.5°C)-induced necroptosis in rat striatal neurons and an in vivo rat model. METH treatment increased core body temperature and up-regulated LDH activity and the molecular expression of canonical necroptotic factors in the striatum of rats. METH and HT can induce necroptosis in primary cultures of striatal neurons. The expression of HSP90α increased following METH/HT injuries. The specific inhibitor of HSP90α, geldanamycin (GA), and HSP90α shRNA attenuated the METH/HT-induced upregulation of receptor-interacting protein 3 (RIP3), phosphorylated RIP3, mixed lineage kinase domain-like protein (MLKL), and phosphorylated MLKL. The inhibition of HSP90α protected the primary cultures of striatal neurons from METH/HT-induced necroptosis. In conclusion, HSP90α plays an important role in METH/HT-induced neuronal necroptosis and the HSP90α-RIP3 pathway is a promising therapeutic target for METH/HT-induced neurotoxicity in the striatum.

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Methamphetamine induces GSDME-dependent cell death in hippocampal neuronal cells through the endoplasmic reticulum stress pathway

Cited by 19 publications

References 63 publications

The Significance of NLRP Inflammasome in Neuropsychiatric Disorders

The Significance of NLRP Inflammasome in Neuropsychiatric Disorders

Molecular mechanisms of programmed cell death in methamphetamine-induced neuronal damage

The Role of HSP90α in Methamphetamine/Hyperthermia-Induced Necroptosis in Rat Striatal Neurons

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