Refine
Has Fulltext
- yes (10)
Is part of the Bibliography
- yes (10)
Document Type
- Journal article (10)
Language
- English (10)
Keywords
- HBMEC (3)
- Ureaplasma parvum (3)
- blood–brain barrier (3)
- Ureaplasma urealyticum (2)
- endoglin (2)
- hypoxia (2)
- meningitis (2)
- multiple sclerosis (2)
- neuroinflammation (2)
- stroke (2)
- ASC (1)
- Apoptosis (1)
- Biomarker (1)
- CD105 (1)
- CNS integrity (1)
- CXCL5 (1)
- CXCL8 (1)
- CXCR2 (1)
- Caspase (1)
- Cell Index (1)
- Gehirn (1)
- MCC950 (1)
- Meningitis (1)
- NF-\(\kappa\)B (1)
- NLRP3 (1)
- Neuroinflammation (1)
- SB332235 (1)
- Ureaplasma species (1)
- VCAM-1 (1)
- animal model (1)
- atypical chemokine receptor 3 (1)
- barrier integrity (1)
- biomarker (1)
- blood-brain barrier (1)
- brain endothelium (1)
- cell adhesion (1)
- dimethyl fumarate (1)
- drug (1)
- endothelial cells (1)
- gene (1)
- human brain endothelium (1)
- human brain microvascular endothelial cells (1)
- human cerebral endothelial cells (1)
- i.v. thrombolysis (1)
- immaturity (1)
- inflammasome (1)
- interleukin-8 (1)
- ischemia/reperfusion injury (1)
- ischemic stroke (1)
- mechanical thrombectomy (1)
- middle cerebral artery occlusion (1)
- monomethyl fumarate (1)
- neonatal meningitis (1)
- p38 mitogen-activated protein kinase (1)
- potent inducer (1)
- preterm birth (1)
- proteins (1)
- reoxygenation (1)
- reperfusion injury (1)
- rt-PA (1)
- shedding (1)
- soluble endoglin (1)
- vascular homeostasis (1)
Institute
- Neurologische Klinik und Poliklinik (10)
- Kinderklinik und Poliklinik (6)
- Institut für Hygiene und Mikrobiologie (3)
- Klinik und Poliklinik für Allgemein-, Viszeral-, Gefäß- und Kinderchirurgie (Chirurgische Klinik I) (2)
- Institut für Klinische Epidemiologie und Biometrie (1)
- Institut für diagnostische und interventionelle Neuroradiologie (ehem. Abteilung für Neuroradiologie) (1)
- Pathologisches Institut (1)
Sonstige beteiligte Institutionen
Background: An inducible release of soluble junctional adhesion molecule-A (sJAM-A) under pro-inflammatory conditions was described in cultured non-CNS endothelial cells (EC) and increased sJAM-A serum levels were found to indicate inflammation in non-CNS vascular beds. Here we studied the regulation of JAM-A expression in cultured brain EC and evaluated sJAM-A as a serum biomarker of blood-brain barrier (BBB) function. Methodology/Principal Findings: As previously reported in non-CNS EC types, pro-inflammatory stimulation of primary or immortalized (hCMEC/D3) human brain microvascular EC (HBMEC) induced a redistribution of cell-bound JAM-A on the cell surface away from tight junctions, along with a dissociation from the cytoskeleton. This was paralleled by reduced immunocytochemical staining of occludin and zonula occludens-1 as well as by increased paracellular permeability for dextran 3000. Both a self-developed ELISA test and Western blot analysis detected a constitutive sJAM-A release by HBMEC into culture supernatants, which importantly was unaffected by pro-inflammatory or hypoxia/reoxygenation challenge. Accordingly, serum levels of sJAM-A were unaltered in 14 patients with clinically active multiple sclerosis compared to 45 stable patients and remained unchanged in 13 patients with acute ischemic non-small vessel stroke over time. Conclusion: Soluble JAM-A was not suited as a biomarker of BBB breakdown in our hands. The unexpected non-inducibility of sJAM-A release at the human BBB might contribute to a particular resistance of brain EC to inflammatory stimuli, protecting the CNS compartment.