ArticleMolecular neurobiology2017
Roles of HIF-1α, VEGF, and NF-κB in Ischemic Preconditioning-Mediated Neuroprotection of Hippocampal CA1 Pyramidal Neurons Against a Subsequent Transient Cerebral Ischemia.
Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 44 citations in OpenAlex.
- Repetitive hypoxic preconditioning protects retinal ganglion cells against damage caused by exposure to blast.PloS one · 2026Article
- Reciprocal regulation of GPNMB/HIF-1α for Inhibition of neuronal ferroptosis in delayed encephalopathy after acute carbon monoxide poisoning.Acta neuropathologica communications · 2025Article
- Bacopa monnieri Extract Diminish Hypoxia-Induced Anxiety by Regulating HIF-1α Signaling and Enhancing the Antioxidant Defense System in Hippocampus.Neuromolecular medicine · 2025Article
- HIF-1α knockdown attenuates inflammation and oxidative stress in ischemic stroke male rats via CXCR4/NF-κB pathway.Brain and behavior · 2024Article
- Compound Shenma Jingfu granule alleviates cerebral ischemia via HIF-1α-mediated promotion of angiogenesis.Chinese medicine · 2024Article
- Research hotspots and frontiers of preconditioning in cerebral ischemia: A bibliometric analysis.Heliyon · 2024Review
- Cortical microinfarcts potentiate recurrent ischemic injury through NLRP3-dependent trained immunity.Cell death & disease · 2024Article
- Review
- Hyperthermia accelerates neuronal loss differently between the hippocampal CA1 and CA2/3 through different HIF‑1α expression after transient ischemia in gerbils.International journal of molecular medicine · 2022Article
- HIF‑1α in cerebral ischemia (Review).Molecular medicine reports · 2022Review
- Association of time to groin puncture with patient outcome after endovascular therapy stratified by etiology.Frontiers in aging neuroscience · 2022Article
- Molar loss further exacerbates 2-VO-induced cognitive impairment associated with the activation of p38MAPK/NFκB pathway.Frontiers in aging neuroscience · 2022Article
- Article
- MUC3A promotes non-small cell lung cancer progression via activating the NFκB pathway and attenuates radiosensitivity.International journal of biological sciences · 2021Article
- Hypoxia-Inducible Factor (HIF) in Ischemic Stroke and Neurodegenerative Disease.Frontiers in cell and developmental biology · 2021Review
- Exploring the Regulatory Mechanism ofFrontiers in pharmacology · 2021Article
- Dimethyloxalyl Glycine Regulates the HIF-1 Signaling Pathway in Mesenchymal Stem Cells.Stem cell reviews and reports · 2020Article
- Review Cerebral Ischemic Tolerance and Preconditioning: Methods, Mechanisms, Clinical Applications, and Challenges.Frontiers in neurology · 2020Review
- Article
- Preactivation of Notch1 in remote ischemic preconditioning reduces cerebral ischemia-reperfusion injury through crosstalk with the NF-κB pathway.Journal of neuroinflammation · 2019Article
Corrections and comments
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Authors and funding
17 authors at 7 institutions in 3 countries.
Funding
Abstract
Ischemic preconditioning (IPC) provides neuroprotection against subsequent severe ischemic insults by specific mechanisms. We tested the hypothesis that IPC attenuates post-ischemic neuronal death in the gerbil hippocampal CA1 region (CA1) throughout hypoxia inducible factor-1α (HIF-1α) and its associated factors such as vascular endothelial growth factor (VEGF) and nuclear factor-kappa B (NF-κB). Lethal ischemia (LI) without IPC increased expressions of HIF-1α, VEGF, and p-IκB-α (/and translocation of NF-κB p65 into nucleus) in CA1 pyramidal neurons at 12 h and/or 1-day post-LI; thereafter, their expressions were decreased in the CA1 pyramidal neurons with time and newly expressed in non-pyramidal cells (pericytes), and the CA1 pyramidal neurons were dead at 5-day post-LI, and, at this point in time, their immunoreactivities were newly expressed in pericytes. In animals with IPC subjected to LI (IPC/LI)-group), CA1 pyramidal neurons were well protected, and expressions of HIF-1α, VEGF, and p-IκB-α (/and translocation of NF-κB p65 into nucleus) were significantly increased compared to the sham-group and maintained after LI. Whereas, treatment with 2ME2 (a HIF-1α inhibitor) into the IPC/LI-group did not preserve the IPC-mediated increases of HIF-1α, VEGF, and p-IκB-α (/and translocation of NF-κB p65 into nucleus) expressions and did not show IPC-mediated neuroprotection. In brief, IPC protected CA1 pyramidal neurons from LI by upregulation of HIF-1α, VEGF, and p-IκB-α expressions. This study suggests that IPC increases HIF-1α expression in CA1 pyramidal neurons, which enhances VEGF expression and NF-κB activation and that IPC may be a strategy for a therapeutic intervention of cerebral ischemic injury.
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