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Concussive injury elicits human cerebrovascular endothelial cell activation in vitro
Author(s) -
Augustine Claudia,
Cepinskas Gediminas,
Fraser Douglas
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.650.10
Subject(s) - medicine , traumatic brain injury , anesthesia , in vitro , nitric oxide , reactive oxygen species , chemistry , biochemistry , psychiatry
Concussive brain injury may directly injure cerebrovascular endothelial cells (CVEC) of the blood‐brain barrier and/or CVEC may be altered by circulating trauma‐induced inflammatory mediators. Thus, we assessed for activation of CVEC by either a concussive injury or by application of plasma from trauma patients. Methods Plasma was obtained from pediatric multisystem trauma patients (injury severity score≥12) and age/sex‐matched controls. Human immortalized CVEC (hCMEC/D3; provided by Dr. P. Couraud, INSERM) were employed to assess for activation in vitro . Concussive injury was induced in hCMEC/D3 grown on flexible supports with a compressed air pulse at 4 psi/well. In parallel, uninjured CVEC were treated with 20% v/v blood plasma collected from trauma patients or healthy controls. Results A single concussive injury to hCMEC/D3 resulted in increased nitric oxide (NO; DAF‐FM nitrosation) at 15 and 30 minutes, increased reactive oxygen species (ROS; DHR‐123 oxidation) at 2 hours and increased 51 Cr‐PMN adhesion at 6 hours. In contrast, application of 20% v/v trauma patient plasma to hCMEC/D3 failed to induce oxidative stress, activate NF‐κB (ELISA) or elicit PMN adhesion assessed under “flow” (relative to control plasma‐treated hCMEC/D3). Conclusions Direct concussive injury induces hCMEC/D3 activation in vitro , whereas application of 20% v/v trauma plasma is not potent enough to activate CVEC.