Acetylcholine induces intracellular Ca2+ oscillations and nitric oxide release in mouse brain endothelial cells

Cell Calcium ◽  
2017 ◽  
Vol 66 ◽  
pp. 33-47 ◽  
Author(s):  
Estella Zuccolo ◽  
Dmitry Lim ◽  
Dlzar Ali Kheder ◽  
Angelica Perna ◽  
Paolo Catarsi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Mouse Brain ◽  
Brain Endothelial Cells ◽  
Nitric Oxide Release ◽  
Mouse Brain Endothelial Cells

In vivoradioprotection of mouse brain endothelial cells by Hoechst 33342

2001 ◽  
Vol 74 (877) ◽  
pp. 77-82 ◽  
Author(s):  
N V Lyubimova ◽  
P G Coultas ◽  
K Yuen ◽  
R F Martin
Keyword(s):  
Endothelial Cells ◽  
Mouse Brain ◽  
Brain Endothelial Cells ◽  
Hoechst 33342 ◽  
Mouse Brain Endothelial Cells

scholarly journals Mouse Adenovirus Type 1-Induced Breakdown of the Blood-Brain Barrier

2009 ◽  
Vol 83 (18) ◽  
pp. 9398-9410 ◽  
Author(s):  
Lisa E. Gralinski ◽  
Shanna L. Ashley ◽  
Shandee D. Dixon ◽  
Katherine R. Spindler
Keyword(s):  
Endothelial Cells ◽  
Blood Brain Barrier ◽  
Mouse Brain ◽  
Adenovirus Type ◽  
Brain Barrier ◽  
Brain Endothelial Cells ◽  
Blood Brain ◽  
Mouse Brain Endothelial Cells ◽  
Primary Mouse ◽  
Infected Cells

ABSTRACT Infection with mouse adenovirus type 1 (MAV-1) results in fatal acute encephalomyelitis in susceptible mouse strains via infection of brain endothelial cells. Wild-type (wt) MAV-1 causes less brain inflammation than an early region 3 (E3) null virus in C57BL/6 mice. A mouse brain microvascular endothelial cell line infected with wt MAV-1 had higher expression of mRNAs for the proinflammatory chemokines CCL2 and CCL5 than mock- and E3 null virus-infected cells. Primary mouse brain endothelial cells infected with wt virus had elevated levels of CCL2 compared to mock- or E3 null virus-infected cells. Infection of C57BL/6 mice with wt MAV-1 or the E3 null virus caused a dose-dependent breakdown of the blood-brain barrier, primarily due to direct effects of virus infection rather than inflammation. The tight junction proteins claudin-5 and occludin showed reduced surface expression on primary mouse brain endothelial cells following infection with either wt MAV-1 or the E3 null virus. mRNAs and protein for claudin-5, occludin, and zona occludens 2 were also reduced in infected cells. MAV-1 infection caused a loss of transendothelial electrical resistance in primary mouse brain endothelial cells that was not dependent on E3 or on MAV-1-induced CCL2 expression. Taken together, these results demonstrate that MAV-1 infection caused breakdown of the blood-brain barrier accompanied by decreased surface expression of tight junction proteins. Furthermore, while the MAV-1-induced pathogenesis and inflammation were dependent on E3, MAV-1-induced breakdown of the blood-brain barrier and alteration of endothelial cell function were not dependent on E3 or CCL2.

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