ArticleJournal of neurochemistry2011
C5a/CD88 signaling alters blood-brain barrier integrity in lupus through nuclear factor-κB.
Article in Journal of neurochemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
33 citing papers in PubMed, 60 citations in OpenAlex.
- Immunopathogenesis of neuropsychiatric systemic lupus erythematosus: current insights into inflammatory and thrombotic pathways.Journal of neuroinflammation · 2026Review
- Emerging role of complement system in the induction of neuroinflammation in adenylosuccinate lyase deficiency disorder.Brain, behavior, & immunity - health · 2025Review
- Review
- The role of vitamin D: a promising pathway to combat neuropsychiatric lupus disorders.Clinical and experimental immunology · 2025Article
- C3a Mediates Endothelial Barrier Disruption in Brain-Derived, but Not Retinal, Human Endothelial Cells.International journal of molecular sciences · 2024Article
- Choroid plexus and perivascular space enlargement in neuropsychiatric systemic lupus erythematosus.Molecular psychiatry · 2024Article
- A20 regulates lymphocyte adhesion in murine neuroinflammation by restricting endothelial ICOSL expression in the CNS.The Journal of clinical investigation · 2023Article
- Complement: Functions, location and implications.Immunology · 2023Review
- Exploring Pro-Inflammatory Immunological Mediators: Unraveling the Mechanisms of Neuroinflammation in Lysosomal Storage Diseases.Biomedicines · 2023Review
- Complementing Testicular Immune Regulation: The Relationship between Sertoli Cells, Complement, and the Immune Response.International journal of molecular sciences · 2023Review
- Targeting the Complement-Sphingolipid System in COVID-19 and Gaucher Diseases: Evidence for a New Treatment Strategy.International journal of molecular sciences · 2022Review
- Insights into the role of neutrophils in neuropsychiatric systemic lupus erythematosus: Current understanding and future directions.Frontiers in immunology · 2022Review
- MERS-CoV infection causes brain damage in human DPP4-transgenic mice through complement-mediated inflammation.The Journal of general virology · 2021Article
- Lupus animal models and neuropsychiatric implications.Clinical rheumatology · 2021Review
- The Role of NETosis in Systemic Lupus Erythematosus.Journal of cellular immunology · 2019Article
- Mesenchymal stem cells alleviate acute kidney injury by down-regulating C5a/C5aR pathway activation.International urology and nephrology · 2018Article
- Relationship between G proteins coupled receptors and tight junctions.Tissue barriers · 2018Review
- Complement C5a Receptor is the Key Initiator of Neutrophil Adhesion Igniting Immune Complex-induced Arthritis.Science immunology · 2017Article
- Sepsis-Associated Encephalopathy: The Blood-Brain Barrier and the Sphingolipid Rheostat.Frontiers in immunology · 2017Review
- C5a induces caspase-dependent apoptosis in brain vascular endothelial cells in experimental lupus.Immunology · 2016Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Inflammation is a key factor in a number of neurodegenerative diseases including systemic lupus erythematosus. The complement system is an important mechanism in initiating and amplifying inflammation. Our recent studies demonstrate that C5a, a protein fragment generated during complement activation could alter the blood-brain barrier integrity, and thereby disturb the brain microenvironment. To understand the mechanism by which this occurs, we examined the effects of C5a on apoptosis, translocation of nuclear factor-κB (NF-κb) and the expression of Iκbα, MAPK, CREB and TJ protein, zona occludens (ZO-1) in mouse brain endothelial cells. Apoptosis was examined by DNA laddering and caspase 3 activity and the distribution of the ZO-1 and the p65 subunit of NF-κB were determined by immunofluorescence. Inhibition of CD88 reduced translocation of NF-κb into the nucleus, altered ZO-1 at the interfaces of neighboring cells, decreased caspase 3 activity and prevented apoptosis in these cells. Our results indicate that signaling through CD88 regulates the blood-brain barrier in a NF-κb-dependent manner. These studies suggest that the C5a receptor, CD88 is a promising therapeutic target that will reduce NF-κb-signaling cascades in inflammatory settings.
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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.