scholarly journals Flavin-Containing Monooxygenase (FMO) Protein Expression and Its Activity in Rat Brain Microvascular Endothelial Cells

2013 ◽  
Vol 04 (01) ◽  
pp. 1-6 ◽  
Author(s):  
Eiichi Sakurai ◽  
Yukari Ueda ◽  
Yukari Mori ◽  
Yasuhumi Shinmyouzu ◽  
Eiko Sakurai
Keyword(s):  
Endothelial Cells ◽  
Protein Expression ◽  
Rat Brain ◽  
Microvascular Endothelial Cells ◽  
Brain Microvascular Endothelial Cells ◽  
Fmo Protein ◽  
Microvascular Endothelial

Expression of Zinc-Finger Antiviral Protein in hCMEC/D3 Human Cerebral Microvascular Endothelial Cells: Effect of a Toll-Like Receptor 3 Agonist

2021 ◽  
pp. 1-10
Author(s):  
Mako Okudera ◽  
Minami Odawara ◽  
Masashi Arakawa ◽  
Shogo Kawaguchi ◽  
Kazuhiko Seya ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Protein Expression ◽  
Zinc Finger ◽  
Microvascular Endothelial Cells ◽  
Brain Microvascular Endothelial Cells ◽  
Toll Like Receptor ◽  
Antiviral Protein ◽  
Polycytidylic Acid ◽  
Microvascular Endothelial ◽  
The Brain

<b><i>Introduction:</i></b> Invasion of viruses into the brain causes viral encephalitis, which can be fatal and causes permanent brain damage. The blood-brain barrier (BBB) protects the brain by excluding harmful substances and microbes. Brain microvascular endothelial cells are important components of the BBB; however, the mechanisms of antiviral reactions in these cells have not been fully elucidated. Zinc-finger antiviral protein (ZAP) is a molecule that restricts the infection of various viruses, and there are 2 major isoforms: ZAPL and ZAPS. Toll-like receptor 3 (TLR3), a pattern-recognition receptor against viral double-stranded RNA, is implicated in antiviral innate immune reactions. The aim of this study was to investigate the expression of ZAP in cultured hCMEC/D3 human brain microvascular endothelial cells treated with an authentic TLR3 agonist polyinosinic-polycytidylic acid (poly IC). <b><i>Methods:</i></b> hCMEC/D3 cells were cultured and treated with poly IC. Expression of ZAPL and ZAPS mRNA was investigated using quantitative reverse transcription-polymerase chain reaction, and protein expression of these molecules was examined using western blotting. The role of nuclear factor-κB (NF-κB) was examined using the NF-κB inhibitor, SN50. The roles of interferon (IFN)-β, IFN regulatory factor 3 (IRF3), tripartite motif protein 25 (TRIM25), and retinoic acid-inducible gene-I (RIG-I) in poly IC-induced ZAPS expression were examined using RNA interference. Propagation of Japanese encephalitis virus (JEV) was examined using a focus-forming assay. <b><i>Results:</i></b> ZAPS mRNA and protein expression was upregulated by poly IC, whereas the change of ZAPL mRNA and protein levels was minimal. Knockdown of IRF3 or TRIM25 decreased the poly IC-induced upregulation of ZAPS, whereas knockdown of IFN-β or RIG-I did not affect ZAPS upregulation. SN50 did not affect ZAPS expression. Knockdown of ZAP enhanced JEV propagation. <b><i>Conclusion:</i></b> ZAPL and ZAPS were expressed in hCMEC/D3 cells, and ZAPS expression was upregulated by poly IC. IRF3 and TRIM25 are involved in poly IC-induced upregulation of ZAPS. ZAP may contribute to antiviral reactions in brain microvascular endothelial cells and protect the brain from invading viruses such as JEV.

scholarly journals Cocaine inhibits store-operated Ca2+ entry in brain microvascular endothelial cells: critical role for sigma-1 receptors

2015 ◽  
Vol 473 (1) ◽  
pp. 1-5 ◽  
Author(s):  
G. Cristina Brailoiu ◽  
Elena Deliu ◽  
Linda M. Console-Bram ◽  
Jonathan Soboloff ◽  
Mary E. Abood ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Rat Brain ◽  
Critical Role ◽  
Calcium Entry ◽  
Microvascular Endothelial Cells ◽  
Brain Microvascular Endothelial Cells ◽  
Sigma 1 Receptor ◽  
Store Operated Calcium Entry ◽  
Sigma 1 ◽  
Microvascular Endothelial

We provide evidence that cocaine induces sigma-1 receptor-mediated inhibition of store-operated calcium entry (SOCE) in rat brain microvascular endothelial cells. Thus, we reveal sigma-1 receptors as SOCE blockers, adding novel insight regarding endothelial effects of cocaine and endogenous SOCE modulation.

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