Rat Brain Microvascular Endothelial Cells: RBMVEC, adult

RBMVEC from Cell Applications, Inc. provide an excellent model system to study many aspects of endothelial function and disease, especially those related to the blood-brain barrier (BBB), including interactions between neurons, astorcytes and endothelial cells, brain cognitive function, search for therapeutic modulators, and develop novel drug delivery methods for crossing the BBB.RBMVEC from Cell Applications, Inc. have been utilized in a number of research publications, for example to:. Serve as a gold standard control for endothelial markers VE-cadherin and CD31 expression (Johansson, 2009). Demonstrate a better brain penetration of cardiovascular and anti-stroke drugs Tanshinones IIA and IIB and Cryptotanshinone in the presence of PgP or MRP1/2 inhibitors (Chen, 2007; Yu, 2007; Zhi-Wei, 2007) or by using PEGylated gold nanoparticles (Etame, 2011). Show that removal of excess glutamate from the blood by glutamate oxaloacetate transaminase correlates to a decrease in brain glutamate levels and confers neuroprotection against ischemic stroke (Campos, 2011). Assess, along with Rat Astrocytes (RA) also obtained from Cell Applications, Inc., neuroprotective capabilities of bioenergy stabilizers in an in vitro model of stroke (Liu, 2013). Show that bile acids cause activation of Rac1 and phosphorylation of occluding, explaining increased permeability of the blood brain barrier seen during obstructive cholestasis (Quinn, 2014). Demonstrate that saquinavir-associated dementia in HIV-positive patients is exacerbated by smoking due to the BBB disruptive effects of both nicotine and saquinavir, mediated by decrease in Notch-4 expression and increase in ROS (Manda, 2010). Show that treatment with connexin43 mimetic peptide which transiently blocks gap junction function, reduces vascular leak and can be used to treat of central nervous system ischaemia (Danesh-Meyer, 2012). Demonstrate that oxygen and glucose deprivation increase ROS, cytochrome c levels and caspase-3 activity, induce tight junction disruption and actin stress fiber formation, leading to BBB break down (Alluri, 2013). Investigate the interactions between neurons, astorcytes and endothelial cells by showing that exposure to metabolic stress induces tissue-type plasminogen activator release from neurons which induces AMPK activation, membrane recruitment of GLUT1, and GLUT1-mediated glucose uptake in astrocytes and endothelial cells, followed by the synthesis and release of lactic acid from astrocytes, and that the uptake of this lactic acid via the monocarboxylate transporter-2 promotes survival in neurons (An, 2013). Study the proapoptotic and anti-angiogenic role of p75NTR in choroidal neovascularization (Tahiri, 2013)