PMID- 27128638
OWN - NLM
STAT- MEDLINE
DCOM- 20170911
LR  - 20180826
IS  - 1440-1681 (Electronic)
IS  - 0305-1870 (Linking)
VI  - 43
IP  - 8
DP  - 2016 Aug
TI  - Characterisation of a mouse cerebral microvascular endothelial cell line (bEnd.3) 
      after oxygen glucose deprivation and reoxygenation.
PG  - 777-86
LID - 10.1111/1440-1681.12587 [doi]
AB  - Studies have utilised immortalised mouse cerebral endothelial cells (bEnd.3) 
      exposed to oxygen glucose deprivation (OGD) to study blood-brain barrier (BBB) 
      disruption after ischaemia. However, there is a paucity of literature describing 
      the duration of OGD (and reoxygenation [RO]) required to best simulate BBB 
      disruption in vivo. In this study we assessed BBB disruption in bEnd.3 cells 
      after exposure to a range of OGD periods, and also after OGD + RO. Exposure of 
      bEnd.3 monolayers to 4, 6, 16, or 24 hours of OGD resulted in a significant 
      increase in permeability. The hyperpermeability after 16 or 24 hours was 
      associated with decreased expression of tight junction proteins (occludin and 
      claudin-5). Furthermore, there was a decrease in cell viability and increased 
      expression of the pro-apoptotic protein, cleaved caspase-3. Exposure of bEnd.3 
      monolayers to 1 hour OGD+ 23 hours RO exacerbated hyperpermeability relative to 1 
      hour OGD, which was associated with decreased expression levels of occludin and 
      ZO-1, but no change in cell viability or caspase-3. 4 hours OGD + 23 hours RO 
      exacerbated hyperpermeability, decreased expression levels of tight junction 
      proteins, decreased cell viability, and increased caspase-3 expression. Thus, 
      bEnd.3 cells exhibit hyperpermeability, a loss of tight junction proteins, and 
      undergo cell death, after exposure to prolonged periods of OGD. Moreover, they 
      exhibit exacerbated hyperpermeability, a loss of tight junction proteins, and 
      increased expression of caspase-3 after OGD + RO. These findings will facilitate 
      the use of this cell line in studies of BBB disruption and for the testing of 
      therapeutics.
CI  - (c) 2016 John Wiley & Sons Australia, Ltd.
FAU - Ku, Jacqueline M
AU  - Ku JM
AD  - School of Health and Biomedical Sciences, RMIT University, Bundoora, Melbourne, 
      Victoria, Australia.
FAU - Taher, Mohammadali
AU  - Taher M
AD  - School of Health and Biomedical Sciences, RMIT University, Bundoora, Melbourne, 
      Victoria, Australia.
FAU - Chin, Kai Yee
AU  - Chin KY
AD  - School of Health and Biomedical Sciences, RMIT University, Bundoora, Melbourne, 
      Victoria, Australia.
FAU - Grace, Megan
AU  - Grace M
AD  - School of Health and Biomedical Sciences, RMIT University, Bundoora, Melbourne, 
      Victoria, Australia.
FAU - McIntyre, Peter
AU  - McIntyre P
AD  - School of Health and Biomedical Sciences, RMIT University, Bundoora, Melbourne, 
      Victoria, Australia.
FAU - Miller, Alyson A
AU  - Miller AA
AD  - School of Health and Biomedical Sciences, RMIT University, Bundoora, Melbourne, 
      Victoria, Australia.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Australia
TA  - Clin Exp Pharmacol Physiol
JT  - Clinical and experimental pharmacology & physiology
JID - 0425076
RN  - IY9XDZ35W2 (Glucose)
RN  - S88TT14065 (Oxygen)
SB  - IM
MH  - Animals
MH  - Blood-Brain Barrier/metabolism
MH  - Capillary Permeability/*physiology
MH  - Cell Hypoxia/physiology
MH  - Cell Line, Transformed
MH  - Cell Survival/physiology
MH  - Cerebrovascular Circulation/*physiology
MH  - Endothelial Cells/*metabolism
MH  - Glucose/*deficiency
MH  - Mice
MH  - Microvessels/*metabolism
MH  - Oxygen/*metabolism
OTO - NOTNLM
OT  - blood-brain barrier
OT  - cell death
OT  - cultured cells
OT  - ischaemia
OT  - permeability
OT  - tight junctions
EDAT- 2016/04/30 06:00
MHDA- 2017/09/12 06:00
CRDT- 2016/04/30 06:00
PHST- 2015/12/05 00:00 [received]
PHST- 2016/04/17 00:00 [revised]
PHST- 2016/04/26 00:00 [accepted]
PHST- 2016/04/30 06:00 [entrez]
PHST- 2016/04/30 06:00 [pubmed]
PHST- 2017/09/12 06:00 [medline]
AID - 10.1111/1440-1681.12587 [doi]
PST - ppublish
SO  - Clin Exp Pharmacol Physiol. 2016 Aug;43(8):777-86. doi: 10.1111/1440-1681.12587.