ArticleFrontiers in cellular neuroscience2023
Transient ischemic stroke triggers sustained damage of the choroid plexus blood-CSF barrier.
Article in Frontiers in cellular neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- The Immunologic Function of the Choroid Plexus: A Gateway to Immunomodulatory Therapy in Injury Models of the Central Nervous System.International journal of molecular sciences · 2026Review
- MASH-Associated T Cell Activation and Neuroinflammation: Evidence for a Hepatosystemic Immune Axis.Seminars in liver disease · 2026Review
- Choroid plexus enlargement correlates with cognitive dysfunction and disease progression in Moyamoya disease.Neurosurgical review · 2025Article
- Adenosine AJournal of the American Heart Association · 2025Article
- Critical role of Slc22a8 in maintaining blood-brain barrier integrity after experimental cerebral ischemia-reperfusion.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2025Article
- "Proteinjury": a universal pathological mechanism mediated by cerebrospinal fluid in neurodegeneration and trauma.Frontiers in cell and developmental biology · 2025Review
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuroinflammation is a pathological event associated with many neurological disorders, including dementia and stroke. The choroid plexus (ChP) is a key structure in the ventricles of the brain that secretes cerebrospinal fluid (CSF), forms a blood-CSF barrier, and responds to disease conditions by recruiting immune cells and maintaining an immune microenvironment in the brain. Despite these critical roles, the exact structural and functional changes to the ChP over post-stroke time remain to be elucidated. We induced ischemic stroke in C57BL/6J mice via transient middle cerebral artery occlusion which led to reduction of cerebral blood flow and infarct stroke. At 1-7 days post-stroke, we detected time-dependent increase in the ChP blood-CSF barrier permeability to albumin, tight-junction damage, and dynamic changes of SPAK-NKCC1 protein complex, a key ion transport regulatory system for CSF production and clearance. A transient loss of SPAK protein complex but increased phosphorylation of the SPAK-NKCC1 complex was observed in both lateral ventricle ChPs. Most interestingly, stroke also triggered elevation of proinflammatory
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