Citation

Rosas-Hernandez H, Cuevas E, Escudero-Lourdes C, Lantz SM, Sturdivant NM, Imam SZ, Sarkar S, Slikker W, Paule MG, Balachandran K, Ali SF. Neurosci. Lett. 2018; 672: 123-129.

Affiliation

Division of Neurotoxicology, National Center for Toxicological Research, 3900 NCTR Road, Jefferson, AR, 72079, USA. Electronic address: Syed.Ali@fda.hhs.gov.

Copyright

(Copyright © 2018, Elsevier Publishing)

DOI

10.1016/j.neulet.2018.02.019

PMID

29458086

Abstract

Traumatic brain injury (TBI) occurs when external mechanical forces induce brain damage as result of impact, penetration or rapid acceleration/deceleration that causes deformation of brain tissue. Depending on its severity, TBI can be classified as mild, moderate or severe and can lead to blood-brain barrier (BBB) dysfunction. In the present study, we evaluated the effects of uniaxial high-speed stretch (HSS) at 0, 5, 10 and 15% on a pure culture of primary rat brain endothelial cells as an in vitro model of TBI to the BBB. LDH release, viability and apoptosis analysis, expression of tight junction proteins and endothelial permeability were evaluated 24 hours after a single stretch episode. HSS slightly increased cell death and apoptosis at 10 and 15%, while LDH release was increased only at 15% stretch. Occludin expression was increased at 10% stretch, while claudin-5 expression was increased at 5% stretch, which also decreased the endothelial permeability. In summary, 15% HSS induced low levels of cell death, consistent with mild TBI and very low percentages of HSS (5%) enhanced the BBB properties, promoting the formation of a stronger barrier. These data support the use of 15% HSS as valuable tool in the study of mild TBI to the BBB in vitro.

Published by Elsevier B.V.

Language: en

Keywords

Blood-brain barrier; Cell death; High-speed stretch; Tight junctions; Traumatic brain injury