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.
引用
收藏
页数:6
相关论文
共 25 条
[11]   Stretch-induced injury of cultured neuronal, glial, and endothelial cells - Effect of Polyethylene glycol-conjugated superoxide dismutase [J].
McKinney, JS ;
Willoughby, KA ;
Liang, S ;
Ellis, EF .
STROKE, 1996, 27 (05) :934-940
[12]   INCREASED PROTEOLYTIC ACTIVITY IS RESPONSIBLE FOR THE ABERRANT MORPHOGENETIC BEHAVIOR OF ENDOTHELIAL-CELLS EXPRESSING THE MIDDLE T-ONCOGENE [J].
MONTESANO, R ;
PEPPER, MS ;
MOHLESTEINLEIN, U ;
RISAU, W ;
WAGNER, EF ;
ORCI, L .
CELL, 1990, 62 (03) :435-445
[13]   In vitro central nervous system models of mechanically induced trauma:: A review [J].
Morrison, B ;
Saatman, KE ;
Meaney, DF ;
McIntosh, TK .
JOURNAL OF NEUROTRAUMA, 1998, 15 (11) :911-928
[14]   In Vitro Models of Traumatic Brain Injury [J].
Morrison, Barclay, III ;
Elkin, Benjamin S. ;
Dolle, Jean-Pierre ;
Yarmush, Martin L. .
ANNUAL REVIEW OF BIOMEDICAL ENGINEERING, VOL 13, 2011, 13 :91-126
[15]   Evaluation of the immortalised mouse brain capillary endothelial cell line, b.End3, as an in vitro blood-brain barrier model for drug uptake and transport studies [J].
Omidi, Y ;
Campbell, L ;
Barar, J ;
Connell, D ;
Akhtar, S ;
Gumbleton, M .
BRAIN RESEARCH, 2003, 990 (1-2) :95-112
[16]  
RAYCHAUDHURY A, 1994, J CELL SCI, V107, P39
[17]   A CELL-CULTURE MODEL OF THE BLOOD-BRAIN-BARRIER [J].
RUBIN, LL ;
HALL, DE ;
PORTER, S ;
BARBU, K ;
CANNON, C ;
HORNER, HC ;
JANATPOUR, M ;
LIAW, CW ;
MANNING, K ;
MORALES, J ;
TANNER, LI ;
TOMASELLI, KJ ;
BARD, F .
JOURNAL OF CELL BIOLOGY, 1991, 115 (06) :1725-1735
[18]   Blood-brain barrier breakdown as a therapeutic target in traumatic brain injury [J].
Shlosberg, Dan ;
Benifla, Mony ;
Kaufer, Daniela ;
Friedman, Alon .
NATURE REVIEWS NEUROLOGY, 2010, 6 (07) :393-403
[19]   BREAKDOWN OF THE BLOOD-BRAIN-BARRIER AFTER FLUID PERCUSSION BRAIN INJURY IN THE RAT .2. EFFECT OF HYPOXIA ON PERMEABILITY TO PLASMA-PROTEINS [J].
TANNO, H ;
NOCKELS, RP ;
PITTS, LH ;
NOBLE, LJ .
JOURNAL OF NEUROTRAUMA, 1992, 9 (04) :335-347
[20]  
Thal S. C., 2013, CRIT CARE M IN PRESS