ArticleNeural regeneration research2013
Aquaporin 4 expression and ultrastructure of the blood-brain barrier following cerebral contusion injury.
Article in Neural regeneration research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Astrocytic abnormalities in brain-specificChannels (Austin, Tex.) · 2025Article
- Induced neural stem cells ameliorate blood-brain barrier injury by modulating the calcium signaling pathway of astrocyte in cerebral ischemia-reperfusion rats.Frontiers in cell and developmental biology · 2025Article
- Aquaporins: Gatekeepers of Fluid Dynamics in Traumatic Brain Injury.International journal of molecular sciences · 2024Review
- Aquaporin 8ab is required in zebrafish embryonic intestine development.Acta biochimica et biophysica Sinica · 2022Article
- Acute effects of human protein S administration after traumatic brain injury in mice.Neural regeneration research · 2020Article
- Sleep Disruption Exacerbates and Prolongs the Inflammatory Response to Traumatic Brain Injury.Journal of neurotrauma · 2020Article
- Blood-brainbarrier disruption dictates nanoparticle accumulation following experimental brain injury.Nanomedicine : nanotechnology, biology, and medicine · 2018Article
- Mfsd2a (Major Facilitator Superfamily Domain Containing 2a) Attenuates Intracerebral Hemorrhage-Induced Blood-Brain Barrier Disruption by Inhibiting Vesicular Transcytosis.Journal of the American Heart Association · 2017Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study aimed to investigate aquaporin 4 expression and the ultrastructure of the blood-brain barrier at 2-72 hours following cerebral contusion injury, and correlate these changes to the formation of brain edema. Results revealed that at 2 hours after cerebral contusion and laceration injury, aquaporin 4 expression significantly increased, brain water content and blood-brain barrier permeability increased, and the number of pinocytotic vesicles in cerebral microvascular endothelial cells increased. In addition, the mitochondrial accumulation was observed. As contusion and laceration injury became aggravated, aquaporin 4 expression continued to increase, brain water content and blood-brain barrier permeability gradually increased, brain capillary endothelial cells and astrocytes swelled, and capillary basement membrane injury gradually increased. The above changes were most apparent at 12 hours after injury, after which they gradually attenuated. Aquaporin 4 expression positively correlated with brain water content and the blood-brain barrier index. Our experimental findings indicate that increasing aquaporin 4 expression and blood-brain barrier permeability after cerebral contusion and laceration injury in humans is involved in the formation of brain edema.
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