ArticleMolecular neurobiology2019
Synergistic Inhibition of ERK1/2 and JNK, Not p38, Phosphorylation Ameliorates Neuronal Damages After Traumatic Brain Injury.
Article in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 40 citations in OpenAlex.
- Combined rituximab and magnesium acetyl taurate therapy attenuates neurodegeneration via ERK/c-JNK/P38MAPK signaling modulation in methylmercury-induced amyotrophic lateral sclerosis-like neurotoxicity.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Nrf2 regulates ICAM-1-mediated neutrophil extracellular trap formation after traumatic brain injury.bioRxiv : the preprint server for biology · 2026Article
- Nrf2 activator peptide protects the brain from cerebral vascular dysfunction in alcohol ingestion.JCI insight · 2026Article
- Exploring NanoherbalIranian journal of medical sciences · 2025Article
- Advances in ERK Signaling Pathway in Traumatic Brain Injury: Mechanisms and Therapeutic Potential.Neurochemical research · 2025Review
- ICAM-1 Deletion Using CRISPR/Cas9 Protects the Brain from Traumatic Brain Injury-Induced Inflammatory Leukocyte Adhesion and Transmigration Cascades by Attenuating the Paxillin/FAK-Dependent Rho GTPase Pathway.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Cellular signaling pathways in the nervous system activated by various mechanical and electromagnetic stimuli.Frontiers in molecular neuroscience · 2024Review
- Article
- Vascular endothelial growth factor isoforms differentially protect neurons against neurotoxic events associated with Alzheimer's disease.Frontiers in molecular neuroscience · 2023Article
- Preclinical findings reveal the pharmacological targets of ferulic acid in the treatment of traumatic brain injury.Food science & nutrition · 2022Article
- Identification of miRNA-mRNA regulatory network associated with the glutamatergic system in post-traumatic epilepsy rats.Frontiers in neurology · 2022Article
- Influence of Melatonin on Behavioral and Neurological Function of Rats with Focal Cerebral Ischemia-Reperfusion Injury via the JNK/FoxO3a/Bim Pathway.Computational and mathematical methods in medicine · 2022Article
- Extracellular signal-regulated kinase-dependent phosphorylation of histone H3 serine 10 is involved in the pathogenesis of traumatic brain injury.Frontiers in molecular neuroscience · 2022Article
- Argon Inhalation for 24 h After Closed-Head Injury Does not Improve Recovery, Neuroinflammation, or Neurologic Outcome in Mice.Neurocritical care · 2021Article
- Neuroprotective Effect of α-Mangostin in the Ameliorating Propionic Acid-Induced Experimental Model of Autism in Wistar Rats.Brain sciences · 2021Article
- iTRAQ-based proteomic profiling reveals protein alterations after traumatic brain injury and supports thyroxine as a potential treatment.Molecular brain · 2021Article
- Wnt Pathway: An Emerging Player in Vascular and Traumatic Mediated Brain Injuries.Frontiers in physiology · 2020Review
- Traumatic brain injury-induced downregulation of Nrf2 activates inflammatory response and apoptotic cell death.Journal of molecular medicine (Berlin, Germany) · 2019Article
- Intrahippocampal miR-342-3p inhibition reduces β-amyloid plaques and ameliorates learning and memory in Alzheimer's disease.Metabolic brain disease · 2019Article
- Animal Models of Traumatic Brain Injury and Assessment of Injury Severity.Molecular neurobiology · 2019Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitogen-activated protein (MAP) kinases are serine/threonine protein kinases that play a critical role in signal transduction and are activated by phosphorylation in response to a variety of pathophysiology stimuli. While MAP kinase signaling has a significant role in the pathophysiology of several neurodegenerative diseases, the precise function of activation of MAP kinase in traumatic brain injury (TBI) is unknown. Therefore, it is important to study the role of MAP kinase signaling in TBI-associated neurological ailments. In this study, using an in vitro stretch injury model in rat embryo neuronal cultures and the in vivo fluid percussion injury (FPI) model in rats, we explored the role of MAP kinase signaling in the mechanisms of cell death in TBI. Our study demonstrated that the stretch injury in vitro and FPI in vivo upregulated the phosphorylation of MAP kinase proteins ERK1/2 and JNK, but not p38. Using ERK1/2 inhibitor U0126, JNK inhibitor SP600125, and p38 inhibitor SB203580, we validated the role of MAP kinase proteins in the activation of NF-kB and caspase-3. By immunofluorescence and western blotting, further, we demonstrated the role of ERK1/2 and JNK phosphorylation in neurodegeneration by analyzing cell death proteins annexin V and Poly-ADP-Ribose-Polymerase p85. Interestingly, combined use of ERK1/2 and JNK inhibitors further attenuated the cell death in stretch-injured neurons. In conclusion, this study could establish the significance of MAP kinase signaling in the pathophysiology of TBI and may have significant implications for developing therapeutic strategies using ERK1/2 and JNK inhibitors for TBI-associated neurological complications.
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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.