ArticleNeurobiology of disease2017
DLK silencing attenuated neuron apoptosis through JIP3/MA2K7/JNK pathway in early brain injury after SAH in rats.
Article in Neurobiology of disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
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- miR-210 Regulates Autophagy Through the AMPK/mTOR Signaling Pathway, Reduces Neuronal Cell Death and Inflammatory Responses, and Enhances Functional Recovery Following Cerebral Hemorrhage in Mice.Neurochemical research · 2025Article
- Review
- The MAP3Ks DLK and LZK Direct Diverse Responses to Axon Damage in Zebrafish Peripheral Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- The blood-brain barrier and the neurovascular unit in subarachnoid hemorrhage: molecular events and potential treatments.Fluids and barriers of the CNS · 2022Review
- Acyl-CoA synthetase long chain family member 4 plays detrimental role in early brain injury after subarachnoid hemorrhage in rats by inducing ferroptosis.CNS neuroscience & therapeutics · 2021Article
- Microarray analysis reveals a potential role of lncRNA expression in remote ischemic preconditioning in myocardial ischemia-reperfusion injury.American journal of translational research · 2021Article
- Clinically Precedented Protein Kinases: Rationale for Their Use in Neurodegenerative Disease.Frontiers in aging neuroscience · 2020Review
- Multitasking: Dual Leucine Zipper-Bearing Kinases in Neuronal Development and Stress Management.Annual review of cell and developmental biology · 2019Review
- High-throughput microscopy exposes a pharmacological window in which dual leucine zipper kinase inhibition preserves neuronal network connectivity.Acta neuropathologica communications · 2019Article
- Neuroprotection mediated by the Wnt/Frizzled signaling pathway in early brain injury induced by subarachnoid hemorrhage.Neural regeneration research · 2019Article
- Tristetraprolin attenuates brain edema in a rat model of cerebral hemorrhage.Brain and behavior · 2019Article
- TRPA1 Activation-Induced Myelin Degradation Plays a Key Role in Motor Dysfunction After Intracerebral Hemorrhage.Frontiers in molecular neuroscience · 2019Article
- An axonal stress response pathway: degenerative and regenerative signaling by DLK.Current opinion in neurobiology · 2018Review
- Inhibition of Lats1/p-YAP1 pathway mitigates neuronal apoptosis and neurological deficits in a rat model of traumatic brain injury.CNS neuroscience & therapeutics · 2018Article
- Neuroprotective Effect of Protein Phosphatase 2A/Tristetraprolin Following Subarachnoid Hemorrhage in Rats.Frontiers in neuroscience · 2018Article
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
objectiveDual leucine zipper kinase (DLK/MA3K12) has been reported involved in apoptosis and neuronal degeneration during neural development and traumatic brain injury. This study was designed to investigate the role of DLK with its adaptor protein JNK interacting protein-3 (JIP3), and its downstream MA2K7/JNK signaling pathway in early brain injury (EBI) after subarachnoid hemorrhage (SAH) in a rat model.
designControlled in vivo laboratory study.
settingAnimal research laboratory. SUBJECTS: Two hundred and twenty-three adult male Sprague-Dawley rats weighing 280-320g.
interventionsSAH was induced by endovascular perforation in rats. The SAH grade, neurological score, and brain water content were measured at 24 and 72h after SAH. Immunofluorescence staining was used to detect the cells that expressed DLK. The terminal deoxynucleotid transferase-deoxyuridine triphosphate (dUTP) nick end labeling (TUNEL) was used to detect the neuronal apoptosis. In mechanism research, the expression of DLK, JIP3, phosphorylated-JNK (p-JNK)/JNK, and cleaved caspase-3 (CC-3) were analyzed by western blot at 24h after SAH. The DLK small interfering RNA (siRNA), JIP3 siRNA, MA2K7 siRNA and recombinant DLK protein which injected intracerebroventricularly were given as the interventions. MEASUREMENTS AND MAIN
resultsThe DLK expression was increased in the left cortex neurons and peaked at 24h after SAH. DLK siRNA attenuated brain edema, reduced neuronal apoptosis, and improved the neurobehavioral functions after SAH, but the recombinant DLK protein deteriorated neurobehavioral functions and brain edema. DLK siRNA decreased and recombinant DLK protein increased the expression of MA2K7/p-JNK/CC-3 at 24h after SAH. The JIP3 siRNA reduced the level of JIP3/MA2K7/p-JNK/CC-3, combined DLK siRNA and JIP3 siRNA further decreased the expression of DLK/MA2K7/p-JNK/CC-3, and MA2K7 siRNA lowered the amount of MA2K7/p-JNK/CC-3 at 24h after SAH.
conclusionsAs a negative role, DLK was involved in EBI after SAH, possibly mediated by its adaptor protein JIP3 and MA2K7/JNK signaling pathways. To reduce the level of DLK may be a new target as intervention for SAH.
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