Quantitative Targeted Absolute Proteomic Analysis of Transporters, Receptors and Junction Proteins for Validation of Human Cerebral Microvascular Endothelial Cell Line hCMEC/D3 as a Human Blood–Brain Barrier Model

2012 ◽  
Vol 10 (1) ◽  
pp. 289-296 ◽  
Author(s):  
Sumio Ohtsuki ◽  
Chiemi Ikeda ◽  
Yasuo Uchida ◽  
Yumi Sakamoto ◽  
Florence Miller ◽  
...  
2008 ◽  
Vol 107 (5) ◽  
pp. 1358-1368 ◽  
Author(s):  
Birk Poller ◽  
Heike Gutmann ◽  
Stephan Krähenbühl ◽  
Babette Weksler ◽  
Ignacio Romero ◽  
...  

1997 ◽  
Vol 11 (13) ◽  
pp. 1187-1197 ◽  
Author(s):  
Arumugam Muruganandam ◽  
Leonie Moorhouse Herx ◽  
Robert Monette ◽  
Jon P. Durkin ◽  
Danica B. Stanimirovic

2011 ◽  
Vol 8 (1) ◽  
pp. 71-80 ◽  
Author(s):  
Willem Bintig ◽  
Daniela Begandt ◽  
Barbara Schlingmann ◽  
Linda Gerhard ◽  
Maria Pangalos ◽  
...  

2002 ◽  
Vol 103 (s2002) ◽  
pp. 464S-466S ◽  
Author(s):  
Nicoletta BASILICO ◽  
Livianna SPECIALE ◽  
Silvia PARAPINI ◽  
Pasquale FERRANTE ◽  
Donatella TARAMELLI

In this study, we investigated the production of endothelin 1 (ET-1) by a human microvascular endothelial cell line, HMEC-1, co-cultured with Plasmodium falciparum-parasitized red blood cells (pRBCs). The results indicate that hypoxia increased the basal level of ET-1 production by HMEC-1 cells after 24 or 48h of treatment. However, the co-incubation of HMEC-1 cells with pRBCs, but not with uninfected RBCs, induced a dose-dependent decrease of both constitutive and hypoxia-induced ET-1 production. The inhibition was not due to a decrease in cell viability, as lactate dehydrogenase release remained constant. These results indicate that pRBCs are able to interfere with both the constitutive and stimulated ET-1 release from the microvascular endothelium, thus inducing local modifications of the vascular tone and of the inflammatory response. This could be of relevance in the pathogenesis of the most severe forms of P. falciparum infections, such as cerebral malaria or malaria during pregnancy.


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