Brain Endothelial Cells Activate Neuroinflammatory Pathways in Response to Early Cerebral Small Vessel Disease (CSVD) Patients’ Plasma

The pathogenesis of cerebral small vessel disease (CSVD) is largely unknown. Endothelial disfunction has been suggested as the turning point in CSVD development. In this study, we tested the effect of plasma from CSVD patients on human cerebral microvascular endothelial cells with the aim of describ...

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Bibliographic Details
Published in:Biomedicines 2023-11, Vol.11 (11), p.3055
Main Authors: Cifù, Adriana, Janes, Francesco, Mio, Catia, Domenis, Rossana, Pessa, Maria Elena, Garbo, Riccardo, Curcio, Francesco, Valente, Mariarosaria, Fabris, Martina
Format: Article
Language:English
Subjects:
Asymptomatic
Blood & organ donations
Blood donors
Brain
cerebral small vessel disease
Cerebrovascular diseases
cytokines
Disease prevention
Endothelial cells
endothelial dysfunction
Endothelium
Ethylenediaminetetraacetic acid
Gene expression
Inflammation
Instrument industry
Males
MAP kinase
Metabolism
Microvasculature
Mutation
neuroinflammation
Older people
Penicillin
Plasma
Risk factors
RNA
Signal transduction
Vascular diseases
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Summary:The pathogenesis of cerebral small vessel disease (CSVD) is largely unknown. Endothelial disfunction has been suggested as the turning point in CSVD development. In this study, we tested the effect of plasma from CSVD patients on human cerebral microvascular endothelial cells with the aim of describing the pattern of endothelial activation. Plasma samples from three groups of young subjects have been tested: PTs (subjects affected by early stage CSVD); CTRLs (control subjects without abnormalities at MRI scanning); BDs (blood donors). Human Brain Endothelial Cells 5i (HBEC5i) were treated with plasma and total RNA was extracted. RNAs were pooled to reduce gene expression-based variability and NGS analysis was performed. Differentially expressed genes were highlighted comparing PTs, CTRLs and BDs with HBEC5i untreated cells. No significantly altered pathway was evaluated in BD-related treatment. Regulation of p38 MAPK cascade (GO:1900744) was the only pathway altered in CTRL-related treatment. Indeed, 36 different biological processes turned out to be deregulated after PT treatment of HBEC5i, i.e., the cytokine-mediated signaling pathway (GO:0019221). Endothelial cells activate inflammatory pathways in response to stimuli from CSVD patients’ plasma, suggesting the pathogenetic role of neuroinflammation from the early asymptomatic phases of cerebrovascular disease.
ISSN:2227-9059
2227-9059
DOI:10.3390/biomedicines11113055