ArticleTranslational psychiatry2021
proBDNF expression induces apoptosis and inhibits synaptic regeneration by regulating the RhoA-JNK pathway in an in vitro post-stroke depression model.
Article in Translational psychiatry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.
- Non-Invasive Brain Stimulation Progression in Post-Stroke Depression Treatment: A Systematic Review.Alpha psychiatry · 2024Pooled it
- p75 neurotrophin receptor modulation in mild to moderate Alzheimer disease: a randomized, placebo-controlled phase 2a trial.Nature medicine · 2024Trial
- High-Dose MK-801 Attenuated Early TTC-Defined Cortical Injury Even under the Conditions of Suppressed Rapamycin-Sensitive pS6 Signaling during Early Cerebral Ischemia-Reperfusion.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Synaptojanin-2-binding protein ameliorates oxidative stress, neuroinflammation and depression-like behaviors via SYNJ2/PIPRedox biology · 2026Article
- The synaptic triad in depression: how stress-related pathways converge on BDNF, NMDA receptor, and MMP-9.Pharmacological reports : PR · 2026Review
- proBDNF-SorCS2 Axis Suppresses Osteogenesis and Augments Inflammation of Human Periodontal Ligament Stem Cells in Inflammatory Conditions.International dental journal · 2026Article
- Chrono-combined aerobic-resistance exercises as therapeutic approach to reverse neurodegeneration in rat model: a detailed protocol.Frontiers in aging neuroscience · 2026Article
- Advances in the mechanisms of electroacupuncture in the treatment of cerebral ischemia-reperfusion injury.Frontiers in neuroscience · 2026Review
- Article
- Decreased hippocampal neurogenesis and post-stroke depression.Frontiers in psychiatry · 2026Review
- Brain insulin resistance: a key pathological hub linking metabolic and neuropsychiatric comorbidities.Frontiers in aging neuroscience · 2026Review
- Echinocystic Acid Antagonizes Post-Stroke Depression in Mice by Suppressing the JNK/NF-κB Signaling Pathway.Neuropsychiatric disease and treatment · 2026Article
- Mollugin attenuates oxygen-glucose deprivation/reperfusion-induced brain microvascular endothelial cell death and permeability through activation of BDNF/TrkB-modulated Akt pathway.Journal of bioenergetics and biomembranes · 2025Article
- Elucidating the Mechanism of Emodin in Treating Post-Stroke Depression Through Network Pharmacology and Animal Experiments.CNS neuroscience & therapeutics · 2025Article
- Overexpression of BDNF and uPA Combined with the Suppression of Von Hippel-Lindau Tumor Suppressor Enhances the Neuroprotective Activity of the Secretome of Human Mesenchymal Stromal Cells in the Model of Intracerebral Hemorrhage.International journal of molecular sciences · 2025Article
- Function and application of brain‑derived neurotrophic factor precursors (Review).International journal of molecular medicine · 2025Review
- BDNF/proBDNF Interplay in the Mediation of Neuronal Apoptotic Mechanisms in Neurodegenerative Diseases.International journal of molecular sciences · 2025Review
- Jiawei Kongsheng Zhenzhong Pill (JKZP) Alleviates Chronic Cerebral Hypoperfusion-Induced Hippocampal Synaptic Damage via S100A10/tPA/BDNF Pathway.Brain and behavior · 2025Article
- Review
- Innovative strategies for post-stroke depression: integrating traditional Chinese medicine with neurobiological insights, including the gut-brain axis.Frontiers in pharmacology · 2025Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Brain-derived neurotrophic factor (BDNF) plays an important role in the pathophysiology of post-stroke depression (PSD). However, the precise function and potential mechanism of proBDNF, the precursor form of BDNF, are unknown. In our study, a PSD-like model was established by treating neuronal cells with oxygen-glucose deprivation and corticosterone. We found that the protein proBDNF levels were significantly higher in the cortex and hippocampus in the PSD group than in the control group, suggesting that proBDNF plays a role in the pathophysiology of PSD. Furthermore, we re-established the PSD-like cell model using recombinant p75 neurotrophin receptor (p75NTR) or silencing c-Jun N-terminal kinase (JNK), and found that the PSD-induced upregulation of proBDNF was inhibited by recombinant p75NTR and JNK silencing (siJNK), and increased cellular apoptosis. Moreover, the application of recombinant p75NTR and siJNK in the PSD-like cell model significantly reversed the expression of apoptosis-related and depression-related proteins and decreased cellular apoptosis. Our findings suggest that proBDNF is involved in neural plasticity in PSD in vitro. The RhoA-JNK signaling pathway is activated after proBDNF binds to the p75NTR receptor, followed by the expression of apoptosis-related proteins (PSD95, synaptophysin, and P-cofilin), which contribute to PSD progression. The mechanism might involve the promotion of cellular apoptosis and the inhibition of nerve synapses regeneration by proBDNF.
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Registered trials
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 Socratic graph.