Stretch in Brain Microvascular Endothelial Cells (cEND) as an In Vitro Traumatic Brain Injury Model of the Blood Brain Barrier

被引:16
作者
Salvador, Ellaine [1 ]
Neuhaus, Winfried [1 ,2 ]
Foerster, Carola [1 ]
机构
[1] Univ Wurzburg, Zentrum Operat Med, Klin & Poliklin Anasthesiol, Wurzburg, Germany
[2] Univ Vienna, Fac Life Sci, Dept Med Chem, A-1010 Vienna, Austria
来源
JOVE-JOURNAL OF VISUALIZED EXPERIMENTS | 2013年 / 80期
关键词
Medicine; Issue; 80; stretch injury; traumatic brain injury; blood-brain barrier; brain microvascular endothelial cells (cEND); PERMEABILITY; BREAKDOWN; CULTURE; HYPOXIA; TARGET;
D O I
10.3791/50928
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Due to the high mortality incident brought about by traumatic brain injury (TBI), methods that would enable one to better understand the underlying mechanisms involved in it are useful for treatment. There are both in vivo and in vitro methods available for this purpose. In vivo models can mimic actual head injury as it occurs during TBI. However, in vivo techniques may not be exploited for studies at the cell physiology level. Hence, in vitro methods are more advantageous for this purpose since they provide easier access to the cells and the extracellular environment for manipulation. Our protocol presents an in vitro model of TBI using stretch injury in brain microvascular endothelial cells. It utilizes pressure applied to the cells cultured in flexible-bottomed wells. The pressure applied may easily be controlled and can produce injury that ranges from low to severe. The murine brain microvascular endothelial cells (cEND) generated in our laboratory is a well-suited model for the blood brain barrier (BBB) thus providing an advantage to other systems that employ a similar technique. In addition, due to the simplicity of the method, experimental set-ups are easily duplicated. Thus, this model can be used in studying the cellular and molecular mechanisms involved in TBI at the BBB.
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页数:6
相关论文
共 25 条
[1]  
Albert-Weissenberger Christiane, 2010, Exp Transl Stroke Med, V2, P16, DOI 10.1186/2040-7378-2-16
[2]   Critical role of TRPP2 and TRPC1 channels in stretch-induced injury of blood-brain barrier endothelial cells [J].
Berrout, Jonathan ;
Jin, Min ;
O'Neil, Roger G. .
BRAIN RESEARCH, 2012, 1436 :1-12
[3]   Generation of an Immortalized Murine Brain Microvascular Endothelial Cell Line as an In Vitro Blood Brain Barrier Model [J].
Burek, Malgorzata ;
Salvador, Ellaine ;
Foerster, Carola Y. .
JOVE-JOURNAL OF VISUALIZED EXPERIMENTS, 2012, (66)
[4]   Acute alterations in [Ca2+]i in NG108-15 cells subjected to high strain rate deformation and chemical hypoxia: An in vitro model for neural trauma [J].
Cargill, RS ;
Thibault, LE .
JOURNAL OF NEUROTRAUMA, 1996, 13 (07) :395-407
[5]   A NEW MODEL FOR RAPID STRETCH-INDUCED INJURY OF CELLS IN CULTURE - CHARACTERIZATION OF THE MODEL USING ASTROCYTES [J].
ELLIS, EF ;
MCKINNEY, JS ;
WILLOUGHBY, KA ;
LIANG, S ;
POVLISHOCK, JT .
JOURNAL OF NEUROTRAUMA, 1995, 12 (03) :325-339
[6]   Occludin as direct target for glucocorticoid-induced improvement of blood-brain barrier properties in a murine in vitro system [J].
Förster, C ;
Silwedel, C ;
Golenhofen, N ;
Burek, M ;
Kietz, S ;
Mankertz, J ;
Drenckhahn, D .
JOURNAL OF PHYSIOLOGY-LONDON, 2005, 565 (02) :475-486
[7]  
Geddes-Klein D., 2006, J NEUROTRAUM, V23, P93
[8]   Endogenous glutathione protects cerebral endothelial cells from traumatic injury [J].
Gidday, JM ;
Beetsch, JW ;
Park, TS .
JOURNAL OF NEUROTRAUMA, 1999, 16 (01) :27-36
[9]   Progress and limitations in the use of in vitro cell cultures to serve as a permeability screen for the blood-brain barrier [J].
Gumbleton, M ;
Audus, KL .
JOURNAL OF PHARMACEUTICAL SCIENCES, 2001, 90 (11) :1681-1698
[10]  
Hyder AA, 2007, NEUROREHABILITATION, V22, P341