Search results for "BLOOD-BRAIN BARRIER"
showing 10 items of 141 documents
In vitro models of blood-brain barrier set by co-culturing primary pericytes, astrocytes and brain capillary endothelial cells
2010
The blood-brain barrier (BBB) is formed by brain capillary endothelial cells (BCECs) under the effects of the brain microenvironment. BCECs are sealed together by tight junctions (TJs) [2]. We previously found that occludin, one of the main TJ components, is correctly localized at the cell periphery only if BCECs are co-cultured with neurons/astrocytes [1-2]. Moreover, pericytes induce PLA2 protein expression through activation of PKCalpha and the MAPK/ERK cascade in immortalized GP8.3 endothelial cells [3]. In the present work, we analyzed the effects of pericytes and/or astrocytes on survival and differentiation of primary endothelial cells, in the presence of a serum-free medium. To test…
Is Oxidative Stress the Link Between Cerebral Small Vessel Disease, Sleep Disruption, and Oligodendrocyte Dysfunction in the Onset of Alzheimer’s Dis…
2021
Oxidative stress is an early occurrence in the development of Alzheimer’s disease (AD) and one of its proposed etiologic hypotheses. There is sufficient experimental evidence supporting the theory that impaired antioxidant enzymatic activity and increased formation of reactive oxygen species (ROS) take place in this disease. However, the antioxidant treatments fail to stop its advancement. Its multifactorial condition and the diverse toxicological cascades that can be initiated by ROS could possibly explain this failure. Recently, it has been suggested that cerebral small vessel disease (CSVD) contributes to the onset of AD. Oxidative stress is a central hallmark of CSVD and is depicted as …
Synergistic effects of neurons and astrocytes on the differentiation of brain capillary endothelial cells in culture
2003
Brain capillary endothelial cells form a functional barrier between blood and brain, based on the existence of tight junctions that limit paracellular permeability. Occludin is one of the major transmembrane proteins of tight junctions and its peripheral localization gives indication of tight junction formation. We previously reported that RBE4.B cells (brain capillary endothelial cells), cultured on collagen IV, synthesize occludin and correctly localize it at the cell periphery only when cocultured with neurons. In the present study, we describe a three-cell type-culture system that allowed us to analyze the combined effects of neurons and astrocytes on differentiation of brain capillary …
Exercise and lactate production:implication in fatigue and in brain signaling
2016
More than two hundred years after its discovery, lactate still remains an intriguing molecule. Considered for a long time as a waste product of metabolism and the culprit behind muscular fatigue, it was then recognized as an important fuel for many cells. In particular, in the nervous system, it has been proposed that lactate, released by astrocytes in response to neuronal activation, is taken up by neurons, oxidized to pyruvate and used for synthesizing acetyl-CoA to be used for the tricarboxylic acid cycle. More recently, in addition to this metabolic role, the discovery of a specific receptor prompted a reconsideration of its role, and lactate is now seen as a sort of hormone, even invol…
Influence of polyunsaturated fatty acids on Cortisol transport through MDCK and MDCK-MDR1 cells as blood-brain barrier in vitro model.
2011
Abstract Transport across the blood–brain barrier is a relevant factor in the pharmacological action of many drugs and endogenous substances whose action site is located in brain. An overactive P-gp has been suggested to be of relevance for the resistance of the HPA system to be suppressed by glucocorticoids, which is one of the best described biological abnormalities in certain types of depression. PUFA acids have shown clinical efficacy in depressed patients and the hypothesis is that these compounds are able to reduce HPA axis activity as this effect has been shown in animal models of depression. The objective of the present work was (1) to characterize Cortisol transport through MDCK an…
Mechanisms of C-reactive protein-induced blood-brain barrier disruption.
2009
Background and Purpose— Increased mortality after stroke is associated with brain edema formation and high plasma levels of the acute phase reactant C-reactive protein (CRP). The aim of this study was to examine whether CRP directly affects blood–brain barrier stability and to analyze the underlying signaling pathways. Methods— We used a cell coculture model of the blood–brain barrier and the guinea pig isolated whole brain preparation. Results— We could show that CRP at clinically relevant concentrations (10 to 20 μg/mL) causes a disruption of the blood–brain barrier in both approaches. The results of our study further demonstrate CRP-induced activation of surface Fcγ receptors CD16/32 fo…
Fresh cell therapy followed by fatal coma
1986
A 60-year-old woman received a 3-day course of nine injections of “fresh” cells from fetal lamb ovary, placenta, brain (hypothalamus) and liver. There were no immediate complications, but a few days later she developed headache, fever and hemiparesis. She subsequently fell into a coma and died 3 weeks after her fresh cell therapy and 2 weeks after the onset of her clinical symptoms. Autopsy revealed perivenous leucoencephalopathy with a probably steroid-treatment-induced paucity of perivascular inflammation. Fresh cell therapy, clinical symptomatology and morphological findings suggest, though do not prove, that this patient's monophasic and probably immune-mediated disease is a rare and fa…
Effect of the serum from multiple sclerosis patients on an in vitro model of blood-brain barrier.
2008
Multiple sclerosis (MS) is characterized by focal inflammatory demyelination, largely due to autoimmune responses against different components of the myelin sheet. It is also generally accepted that the pathogenesis of MS consists of inflammatory and neurodegenerative phases, where demyelination should produce partially reversible clinical deficits that can remit, due to limited remyelination, while axonal degeneration produces permanent non-remitting clinical damage. It is also assumed that nervous system inflammation is initiated by autoreactive, myelin-specific T cells that permeate the blood-brain barrier and trigger a series of events leading to tissue destruction. In addition to antib…
Lymphatic vessels of the dura mater: a new discovery?
2015
Aspelund et al. discover the presence of a lymphatic vessel network in the dura mater of the mouse brain and show that these dural lymphatic vessels are important for the clearance of macromolecules from the brain.
Co-culture of rat brain cells as a tool for studying cell-cell interactions
2012
Brain capillary endothelial cells (BCECs) form the blood-brain barrier (BBB) in response to interaction with other brain cells (astrocytes, pericytes and neurons). BCECs are characterized by tight junctions (TJ), maturation and stabilization of which require different proteins, such as occludin. When co-cultured with astrocytes and neurons, BCECs were found to form a monolayer resembling the natural BBB: paracellular flux of dopamine and sucrose (i.e. compounds which are unable to cross the BBB in vivo) significantly decreased (1), while the transendothelial electrical resistance (TEER) increased. In these conditions, BCECs produced a larger amount of occludin and tended to localize it at t…