ArticleMolecular medicine reports2015
Expression of aquaporin-4 and pathological characteristics of brain injury in a rat model of traumatic brain injury.
Article in Molecular medicine reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 58 citations in OpenAlex.
- Experimental Study on Changes in the Structure of the Blood-Brain Barrier after Treatment with Bevacizumab for Traumatic Cerebral Edema.Neurocritical care · 2026Article
- Water channel changes in astrocytes associated with buprenorphine administration in a rat model of diffuse traumatic brain injury.Research square · 2026Article
- Propranolol improves cognitive function and glymphatic system recovery through STAT3/MMP2 pathway after TBI.PloS one · 2026Article
- Pathological changes and aquaporin-4 expression after bevacizumab treatment of traumatic penumbra in the rat brain.Scientific reports · 2025Article
- Aquaporins in Acute Brain Injury: Insights from Clinical and Experimental Studies.Biomedicines · 2025Review
- Aquaporin 4 and the endocannabinoid system: a potential therapeutic target in brain injury.Experimental brain research · 2024Review
- Aquaporins: Gatekeepers of Fluid Dynamics in Traumatic Brain Injury.International journal of molecular sciences · 2024Review
- Dysregulated brain-gut axis in the setting of traumatic brain injury: review of mechanisms and anti-inflammatory pharmacotherapies.Journal of neuroinflammation · 2024Review
- Risk factors and predictive model of cerebral edema after road traffic accidents-related traumatic brain injury.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2024Article
- Broadening horizons: ferroptosis as a new target for traumatic brain injury.Burns & trauma · 2024Review
- Astrocyte regulation of extracellular space parameters across the sleep-wake cycle.Frontiers in cellular neuroscience · 2024Review
- Cellular and Molecular Pathophysiology of Traumatic Brain Injury: What Have We Learned So Far?Biology · 2023Review
- Pathophysiology and Neuroimmune Interactions Underlying Parkinson's Disease and Traumatic Brain Injury.International journal of molecular sciences · 2023Review
- Mfsd2a attenuated hypoxic-ischemic brain damage via protection of the blood-brain barrier in mfat-1 transgenic mice.Cellular and molecular life sciences : CMLS · 2023Article
- MicroRNA-mediated regulation of reactive astrocytes in central nervous system diseases.Frontiers in molecular neuroscience · 2022Review
- Cerebral Microcirculation, Perivascular Unit, and Glymphatic System: Role of Aquaporin-4 as the Gatekeeper for Water Homeostasis.Frontiers in neurology · 2021Review
- A Brief Overview of the Cerebrospinal Fluid System and Its Implications for Brain and Spinal Cord Diseases.Frontiers in human neuroscience · 2021Review
- Acute effects of human protein S administration after traumatic brain injury in mice.Neural regeneration research · 2020Article
- Role of Aquaporins in Inflammation-a Scientific Curation.Inflammation · 2020Review
- Modification of the Marmarou model in developing countries.Annals of medicine and surgery (2012) · 2020Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aquaporin 4 (AQP4) is a widely distributed membrane protein, which is found in glial cells, ependymocytes and capillary endothelial cells in the brain, and particularly in the choroid plexus. AQP4 is a key regulator of water metabolism, and changes in its expression following brain injury are associated with pathological changes in the damaged side of the brain; however, the effects of brain injury on AQP4 and injury‑induced pathological changes in the contralateral non‑damaged side of the brain remain to be fully elucidated. In the present study, male Sprague‑Dawley rats were subjected to traumatic brain injury (TBI) and changes in brain water content, the expression of AQP4 expression and pathological characteristics in the damaged and contralateral non‑damaged sides of the brain were examined. In the damaged side of the brain, vasogenic edema appeared first, followed by cellular edema. The aggravated cellular edema in the damaged side of the brain resulted in two periods of peak edema severity. Pathological changes in the contralateral non‑damaged side of the brain occurred later than those in the damaged side; cellular edema appeared first, followed by vasogenic edema, which was alleviated earlier than the cellular edema. AQP4 was downregulated during vasogenic edema, and upregulated during cellular edema. Taken together, these results suggested that the downregulation of AQP4 was a result of vasogenic edema and that the upregulation of AQP4 may have induced cellular edema.
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