%0 Journal Article
%T ATP-binding cassette transporters in immortalised human brain microvascular endothelial cells in normal and hypoxic conditions
%A Christian Lindner
%A Alexander Sigr¨¹ner
%A Franziska Walther
%A Ulrich Bogdahn
%A Pierre O Couraud
%A Gert Schmitz
%A Felix Schlachetzki
%J Experimental & Translational Stroke Medicine
%D 2012
%I BioMed Central
%R 10.1186/2040-7378-4-9
%X We exposed hCMEC/D3 cells to 24 hours of hypoxia alone and to hypoxia followed by 60 min of reoxygenisation as an in vitro model for I/R. Western blot showed mild upregulation of hypoxia inducible factor (HIF-1¦Á) after hypoxia alone and RNA lysates were analysed with a well-established real-time RT-PCR-based TaqMan low-density array detecting 47 of 48 known human ABC transporters.No significant increases of ABC mRNA expression levels were detected neither in hypoxic nor in I/R samples. However, slight decrease of ABCC1 in hypoxic and I/R samples and of ABCA10 and ABCD3 in I/R samples was observed.Our data suggests that hCMEC/D3 cell line and ¨C at the moment ¨C in vitro models in general are a poor basis for stroke research but may be enhanced by co-culturing more cells of the neurovascular unit inducing an overall ischemic response at the BBB.The successful rescue of penumbral brain tissue by rapid reperfusion may be compromised by ischemia/reperfusion injury (I/R) and other secondary events, amongst them post-ischemic inflammatory response, excitotoxicity, excess of reactive oxygen species (ROS), and induction of apoptotic neuronal cell death [1-3]. The cerebral endothelium, which forms the blood¨Cbrain barrier (BBB) in-vivo, may play a crucial role in post-ischemic reperfusion for several reasons: 1.) it is the primary site where reperfusion occurs, 2.) it allows interaction between the brain¡¯s and body¡¯s immune system and, 3.) it strongly interacts with other cell types of the neurovascular unit via cell-cell, cell-matrix and neuro-endocrine cross talk, amongst others, determining the overall cerebral response to ischemia [4-6]. Several studies with I/R stroke models demonstrated a dynamic, even biphasic BBB permeability increase, whereas in clinical stroke neurology only early post-ischemic BBB disruption has been associated with life threatening oedema formation and increased risk of symptomatic intracerebral hemorrhage [7-10]. However, other than BBB tight junct
%K Blood¨Cbrain barrier
%K Ischemia/reperfusion injury
%K Hypoxia-inducible factor
%K Multidrug resistance
%K ABC transporters
%K Stroke
%U http://www.etsmjournal.com/content/4/1/9