ArticleBrain circulation
Activated complement protein C5a does not affect brain-derived endothelial cell viability and zonula occludens-1 levels following oxygen-glucose deprivation.
Article in Brain circulation. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 6 citations in OpenAlex.
- Mechanisms and Therapeutic Targets of Ischemia-Reperfusion Injury in Stroke: A Narrative Review Focusing on Blood-Brain Barrier Dysfunction.Brain sciences · 2026Review
- Diagnostic Value of Inflammatory Biomarkers in Intracranial Venous Thrombosis: A Multi-model Predictive Analysis.Cureus · 2024Article
- C3a Mediates Endothelial Barrier Disruption in Brain-Derived, but Not Retinal, Human Endothelial Cells.International journal of molecular sciences · 2024Article
- D1 receptor-mediated endogenous tPA upregulation contributes to blood-brain barrier injury after acute ischaemic stroke.Journal of cellular and molecular medicine · 2020Article
- C3a Receptor Inhibition Protects Brain Endothelial Cells Against Oxygen-glucose Deprivation/Reperfusion.Experimental neurobiology · 2019Article
- Therapeutic Target and Cell-signal Communication of Chlorpromazine and Promethazine in Attenuating Blood-Brain Barrier Disruption after Ischemic Stroke.Cell transplantation · 2019Article
- Inflammation is correlated with severity and outcome of cerebral venous thrombosis.Journal of neuroinflammation · 2018Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
background and purposeIschemic brain injury induces both functional and structural disarray affecting the blood-brain barrier (BBB) which in return aggravates stroke outcomes. Complement system and its bioactive proteins are important molecular responders to ischemia. C5a protein along with its receptor C5a receptor 1 is a key component of this system with potent pro-inflammatory and chemoattractant properties. The purpose of this study is to investigate the role of C5a protein and its receptor which are believed to participate in the inflammatory response that follows ischemic insult. MATERIALS AND
methodsTo mimic an ischemic
resultsBrain-derived endothelial cell was susceptible to OGD-induced injury in a duration-dependent manner as was the presence of ZO-1 protein. However, the addition of C5a protein had no notable effects even when used at high concentrations up to 100 nM. While OGD led to reduction in ZO-1 protein levels, no change was seen following the addition of C5a. Finally, OGD led unexpectedly to small decreases in NO generation, but this was again unaltered by C5a.
conclusionsOur study suggests that complement system protein C5a may not have a direct role in the disruption of BBB, following brain ischemia. This is in contrary with previous literature that suggests a possible role of this protein in the inflammatory response to ischemia.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.