ArticleNeurotoxicity research2013
The inhibition of ERK activation mediates the protection of necrostatin-1 on glutamate toxicity in HT-22 cells.
Article in Neurotoxicity research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- Necrostatin-1: a promising compound for neurological disorders.Frontiers in cellular neuroscience · 2024Review
- Necroptosis Contributes to LPS-Induced Activation of the Hypothalamic-Pituitary-Adrenal Axis in a Piglet Model.International journal of molecular sciences · 2022Article
- Blocking ERK-DAPK1 Axis Attenuates Glutamate Excitotoxicity in Epilepsy.International journal of molecular sciences · 2022Article
- Preclinical Evidence for the Interplay between Oxidative Stress and RIP1-Dependent Cell Death in Neurodegeneration: State of the Art and Possible Therapeutic Implications.Antioxidants (Basel, Switzerland) · 2021Review
- An Integrative Transcriptomic and Metabolomic Study Revealed That Melatonin Plays a Protective Role in Chronic Lung Inflammation by Reducing Necroptosis.Frontiers in immunology · 2021Article
- RSK3 mediates necroptosis by regulating phosphorylation of RIP3 in rat retinal ganglion cells.Journal of anatomy · 2020Article
- Neuroprotective Effects of Necrostatin-1 Against Oxidative Stress-Induced Cell Damage: an Involvement of Cathepsin D Inhibition.Neurotoxicity research · 2020Article
- Necrostatin-1 protects C2C12 myotubes from CoCl2-induced hypoxia.International journal of molecular medicine · 2018Article
- The Contribution of Necroptosis in Neurodegenerative Diseases.Neurochemical research · 2017Review
- Pin1 Promotes Regulated Necrosis Induced by Glutamate in Rat Retinal Neurons via CAST/Calpain2 Pathway.Frontiers in cellular neuroscience · 2017Article
- Receptor interacting protein 3-induced RGC-5 cell necroptosis following oxygen glucose deprivation.BMC neuroscience · 2015Article
- Liquiritin modulates ERK‑ and AKT/GSK‑3β‑dependent pathways to protect against glutamate‑induced cell damage in differentiated PC12 cells.Molecular medicine reports · 2014Article
- The predominant protective effect of tianeptine over other antidepressants in models of neuronal apoptosis: the effect blocked by inhibitors of MAPK/ERK1/2 and PI3-K/Akt pathways.Neurotoxicity research · 2014Article
- Ischemia-reperfusion injury of the retina is linked to necroptosis via the ERK1/2-RIP3 pathway.Molecular vision · 2014Article
- Neuroprotective effects of paeoniflorin, but not the isomer albiflorin, are associated with the suppression of intracellular calcium and calcium/calmodulin protein kinase II in PC12 cells.Journal of molecular neuroscience : MN · 2013Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Receptor-interacting protein 1 (RIP1), a molecular switch protein from apoptosis to necroptosis, is regarded to play an essential role in necroptotic cell death. Although the increased RIP1 activity induced by tumor necrosis factor α activates mitogen-activated protein kinases (MAPKs) including ERK and leads to apoptotic or necrotic cell death, it is unclear what is the role of ERK during the process of necroptosis. In this study, our data demonstrated that ERK inhibitors U0126 and PD98059 blocked glutamate-induced necroptosis in HT-22 cells, indicating the critical role of ERK activation in necroptosis. Further, we found glutamate treatment increased phosphorylated ERK1/2 level, but the specific necroptosis inhibitor Necrostatin-1 (Nec-1) significantly inhibited the phosphorylation of ERK1 (P44) at 5, 10, and 15 min after glutamate treatment; the phosphorylation of ERK2 (P42) level was also markedly reduced by Nec-1 at 10 min after glutamate treatment. The phosphorylation of JNK and P38, two other MAPK members, were slightly increased after glutamate treatment, but Nec-1 had no inhibitory effect on JNK and P38 activation. Our finding suggested that ERK activation may play an important role in necroptotic cell death and the inhibition of ERK activation mediated the protection of Nec-1 on glutamate-induced necroptosis. Since ERK is considered as a downstream of RIP1, the RIP1/ERK signal pathway may provide new therapeutic avenues for the treatment of ischemia-reperfusion damage and neurodegenerative diseases-containing necroptotic cell death.
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