ArticleBurns & trauma2021
Aquaporin-4 is a potential drug target for traumatic brain injury via aggravating the severity of brain edema.
Article in Burns & trauma, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 39 citations in OpenAlex.
- Perceiving traumatic brain injury from glymphatic system.Molecular psychiatry · 2025Review
- Neutrophil Extracellular Traps Induce Brain Edema Around Intracerebral Hematoma via ERK-Mediated Regulation of MMP9 and AQP4.Translational stroke research · 2025Article
- Aquaporins in Acute Brain Injury: Insights from Clinical and Experimental Studies.Biomedicines · 2025Review
- Neuroprotective Effects of AER-271 in a tMCAO Mouse Model: Modulation of Autophagy, Apoptosis, and Inflammation.Inflammation · 2025Article
- Protective effects of AER-271 in acute-phase radiation-induced brain injury in rats: reduction of brain edema, inflammation, apoptosis and maintenance of blood-brain barrier integrity.Frontiers in pharmacology · 2025Article
- Research progress of propofol in alleviating cerebral ischemia/reperfusion injury.Pharmacological reports : PR · 2024Review
- Effects of Goreisan in the Perioperative Period of Subthalamic Deep Brain Stimulation in Parkinson's Disease.Brain and behavior · 2024Article
- Aquaporin 4 and the endocannabinoid system: a potential therapeutic target in brain injury.Experimental brain research · 2024Review
- Brain-Targeting Emodin Mitigates Ischemic Stroke via Inhibiting AQP4-Mediated Swelling and Neuroinflammation.Translational stroke research · 2024Article
- Aquaporins: Gatekeepers of Fluid Dynamics in Traumatic Brain Injury.International journal of molecular sciences · 2024Review
- Treatment with the vascular endothelial growth factor-A antibody, bevacizumab, has sex-specific effects in a rat model of mild traumatic brain injury.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024Article
- The role of astrocytes in the glymphatic network: a narrative review.Metabolic brain disease · 2024Review
- Ski ameliorates synovial cell inflammation in monosodium iodoacetate-induced knee osteoarthritis.Heliyon · 2024Article
- Deplete and repeat: microglial CSF1R inhibition and traumatic brain injury.Frontiers in cellular neuroscience · 2024Review
- Mannitol inhibits the proliferation of neural stem cell by a p38 mitogen-activated protein kinase-dependent signaling pathway.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2024Article
- Low-intensity open-field blast exposure effects on neurovascular unit ultrastructure in mice.Acta neuropathologica communications · 2023Article
- Altered endocannabinoid metabolism compromises the brain-CSF barrier and exacerbates chronic deficits after traumatic brain injury in mice.Experimental neurology · 2023Article
- Elucidating the neuroimmunology of traumatic brain injury: methodological approaches to unravel intercellular communication and function.Frontiers in cellular neuroscience · 2023Review
- Progress Toward a Multiomic Understanding of Traumatic Brain Injury: A Review.Biomarker insights · 2022Review
- Aquaporin-4 Mediates Permanent Brain Alterations in a Mouse Model of Hypoxia-Aged Hydrocephalus.International journal of molecular sciences · 2021Article
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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
backgroundTraumatic brain edema (TBE) is caused by a specific water channel mediated by membrane aquaporins. Aquaporin-4 (AQP4) plays an especially important role in this process, but the relationship between AQP4 and TBE remains unclear. The purpose of this study was to explore expression of AQP4 in the hippocampus after traumatic brain injury (TBI), as well as the effect of brain edema on skeletal protein and its function in hippocampal neurons.
methodsThe adult male Wistar rats we divided into a sham group and a TBI group, the latter of which was further divided into 1, 3, 6, 12, 24 and 72 hours (h) and 15 days (d) post injury subgroups. A proper TBI model was established, and brain edema was assessed in each group by water content. We measured the abundance of various proteins, including hypoxia inducible factor-1α (HIF-1α), AQP4, microtubule-associated protein 2 (MAP2), tau-5 protein, phosphorylated level of TAU, synaptophysin, cyclic adenosine monophosphate response element binding protein (CREB), phosphorylated CREB and general control nonrepressed 2, in each group. Hippocampal neurons and spatial memory test were analyzed in different time points.
resultsCompared with that in the sham group, the level of AQP4 in hippocampal neurons began to significantly increase at 1 h post TBI and then decreased at 15 d post TBI. During this time frame, AQP4 level peaked at 12 and 72 h, and these peaks were closely correlated with high brain water content. HIF-1α displayed a similar trend. Conversely, levels of MAP2 began to decrease at 1 h post TBI and then increase at 15 d post TBI. In addition, the most severe brain edema in rats was found at 24 h post TBI, with neuronal loss and hippocampal dendritic spine injury. Compared to those in the sham group, rats in the TBI groups had significantly prolonged latency and significantly shortened exploration time.
conclusionsAQP4 level was closely correlated with severity of brain edema, and abnormal levels thereof aggravated such severity after TBI.
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