TY - JOUR. T1 - Hydrophilic bile acids protect human blood-brain barrier endothelial cells from disruption by unconjugated bilirubin. T2 - An in vitro study. AU - Palmela, Inês. AU - Correia, Leonor. AU - Silva, Rui F M. AU - Sasaki, Hiroyuki. AU - Kim, Kwang Sik. AU - Brites, Dora. AU - Brito, Maria A.. PY - 2015. Y1 - 2015. N2 - Ursodeoxycholic acid and its main conjugate glycoursodeoxycholic acid are bile acids with neuroprotective properties. Our previous studies demonstrated their anti-apoptotic, anti-inflammatory and antioxidant properties in neural cells exposed to elevated levels of unconjugated bilirubin as in severe jaundice. In a simplified model of the blood-brain barrier, formed by confluent monolayers of a cell line of human brain microvascular endothelial cells, unconjugated bilirubin has shown to induce caspase-3 activation and cell death, as well as interleukin-6 release and a loss of blood-brain barrier integrity. Here we tested the preventive and restorative effects of these ...
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One of the largest and fastest growing sectors in the global pharmaceutical industry is the development of treatments for diseases of the central nervous system. Unfortunately, current systemically administered medications do not achieve optimum therapeutic efficacy in the brain due to limitations in crossing the blood-brain barrier (BBB). Further research is needed to enhance the understanding of how and what molecules can pass through the BBB, and the creation of an in vitro BBB model is crucial to study the cellular constituents and the dynamic capabilities of the BBB that are difficult or nearly impossible to resolve in vivo. The most prevalent BBB model consists of a monolayer of endothelial cells grown on a porous membrane submerged in the wells of a multi-well plate. The large range of cell types available, cell culture variable set points (species, generation, co-culture setup), and system variable set points (membrane configuration, media composition) has resulted in an expansive number ...
TY - JOUR. T1 - Triglyceride-Rich lipoprotein lipolysis products increase Blood-Brain barrier transfer coefficient and induce astrocyte lipid droplets and cell stress. AU - Lee, Linda L.. AU - Aung, Hnin H.. AU - Wilson, Dennis W. AU - Anderson, Steven E.. AU - Rutledge, John C. AU - Rutkowsky, Jennifer M.. PY - 2017/4/7. Y1 - 2017/4/7. N2 - Elevation of blood triglycerides, primarily as triglyceride-rich lipoproteins (TGRL), has been linked to cerebrovascular inflammation, vascular dementia, and Alzheimers disease (AD). Brain microvascular endothelial cells and astrocytes, two cell components of the neurovascular unit, participate in controlling bloodbrain barrier (BBB) permeability and regulating neurovascular unit homeostasis. Our studies showed that infusion of high physiological concentrations of TGRL lipolysis products (TGRL + lipoprotein lipase) activate and injure brain endothelial cells and transiently increase the BBB transfer coefficient (Ki = permeability × surface area/volume) in ...
Quantitative MRI reveals the elderly ischemic brain is susceptible to increased early blood-brain barrier permeability following tissue plasminogen activator related to claudin 5 and occludin disassembly
BACKGROUND: Blood brain barrier (BBB) disruption is accompanied by edema in the surrounding areas of the intracerebral hemorrhage (ICH). The aim of the study was to clarify the correlation between BBB breakdown and outcome in ICH. PATIENTS: Twenty-se
Results: A total of 212 patients, mean age (±SD) 69.5 years (±16.1), 102 (48%) male, had available MR before IV thrombolysis. Evidence of BBB leakage was present in 175 (80%) and 205 (94%) patients in the ischemic and nonischemic area, respectively. Lacunar infarcts (β = 0.17, p = 0.042) were associated with BBB leakage in the ischemic area, and brain atrophy was associated with BBB leakage in both ischemic (β = 0.20, p = 0.026) and nonischemic (β = 0.27, p = 0.001) areas. Increasing SVD grade was independently associated with BBB leakage in both ischemic (β = 0.26, p = 0.007) and nonischemic (β = 0.27, p = 0.003) area. ...
TY - JOUR. T1 - Penetration of small molecular weight substances through cultured bovine brain capillary endothelial cell monolayers. T2 - the early effects of cyclic adenosine 3,5‐monophosphate. AU - Deli, MA. AU - Dehouck, MP. AU - Abraham, CS. AU - Cecchelli, R.. AU - Joo, F.. PY - 1995/7/1. Y1 - 1995/7/1. N2 - Second messengers, such as cyclic adenosine 3,5‐monophosphate (cAMP), have been shown to take part in the regulation of blood‐brain barrier permeability. in the present study, elevation of cAMP levels decreased sucrose (mol. wt, 342) and inulin (mol. wt, 5000) permeability across monolayers of bovine brain capillary endothelial cells as early as 1 h after exposure. Since both tracers use predominantly a paracellular pathway, we assume that cAMP may increase the tightness of the tight junctions through protein phosphorylation.. AB - Second messengers, such as cyclic adenosine 3,5‐monophosphate (cAMP), have been shown to take part in the regulation of blood‐brain barrier ...
Our group recently verified that morphine pre-treatment facilitates doxorubicin delivery beyond the blood brain barrier (BBB) to the brain in the absence of signs of increased acute systemic toxicity in a rat model. Thus, it was plausible that morphine and other drugs as ondansetron inhibiting P-gp (MDR-1) localized on BBB, neurons and glial cells could increase the access of doxorubicin to the brain competing with the same efflux transporter, that very efficiently removes these drugs from the CNS. Thus, we explored the feasibility of active modification of the BBB protection, by using ondansetron pretreatment, to allow doxorubicin accumulation into the brain in an animal model. Rats were pretreated with different doses of intraperitoneal ondansetron before injection of doxorubicin (12 mg/kg). Quantitative analysis of doxorubicin was performed by mass spectrometry. Acute hearth and kidney damage was analyzed by measuring doxorubicin accumulation, LDH activity and malondialdehyde plasma levels. ...
Title: ABC Transporters and the Blood-Brain Barrier. VOLUME: 10 ISSUE: 12. Author(s):David J. Begley. Affiliation:Centre for Neuroscience Research, Kings College London, Hodgkin Building, Guys Campus, London SE1 1UL,UK.. Keywords:abc transporters, blood-brain barrier, blood-cerebrospinal fluid barrier. Abstract: The blood-brain barrier (BBB) and the blood-cerebrospinal fluid barrier (BCSFB) form a very effective barrier to the free diffusion of many polar solutes into the brain. Many metabolites that are polar have their brain entry facilitated by specific inwardly-directed transport mechanisms. In general the more lipid soluble a molecule or drug is, the more readily it will tend to partition into brain tissue. However, a very significant number of lipid soluble molecules, among them many useful therapeutic drugs have lower brain permeability than would be predicted from a determination of their lipid solubility. These molecules are substrates for the ABC efflux transporters which are present ...
The main pathophysiological factors of ICH include hematoma size and edema [38]. The formation of edema, which is mainly caused by disruption of the BBB following ICH, is associated with patient outcome. The BBB is composed of endothelial cells, tight junction proteins, astrocyte end-feet, and pericytes, which have the function of maintaining homeostasis of the neuro-parenchymal microenvironment [6]. Loss of BBB integrity is an important pathophysiological change that contributes to initiation of the inflammatory cascade, edema formation, and ultimately poor outcome [39]. In this study, the effect of MSCs on BBB leakage in ICH rats and relevant mechanisms were investigated after intravenous transplantation of MSCs.. Besides endothelial cell activation, vascular ONOO−, which is formed by NO and superoxide anion, is closely related to BBB leakage [37]. Studies have already shown that ONOO− alone is sufficient to induce BBB leakage, endothelial dysfunction, and neurodegeneration [40,41]. ...
Impaired blood-brain barrier function represents a significant component of hypoxic-ischemic brain injury in the perinatal period. Banks, W. A., Stonestreet, B. S. AntiCIL-6 neutralizing antibody modulates blood-brain barrier function in the ovine fetus. mAb attenuate ischemia-reperfusionCrelated increases in BBB permeability in sheep fetuses (16). However, the role of IL-6 after injury in the immature brain has been studied much less extensively than those of IL-1and TNF-in the immature brain. We recently generated pharmacologic quantities of a highly selective, ovine-specific antiCIL-6 mAb and antiCIL-1mAb. The neutralizing abilities of these mAbs have previously been confirmed in ovine splenic mononuclear cell cultures (35). Moreover, we recently demonstrated that infusions of an antiCIL-1mAb result in the uptake of the antiCIL-1mAb into the brain and attenuate ischemia-reperfusionCrelated increases in BBB permeability in ovine fetal brain using the preclinical translational fetal sheep model ...
Dear Colleagues,. We would like to inform you that the registration and abstract submission for the 20th International Symposium on Signal Transduction at the Blood-Brain Barriers is open till 31st of July and we are looking forward to your registration!. The symposium will be held September 13-15, 2017 in Kraków, Poland.. For more information please see: http://bbb.pan.olsztyn.pl/. The program covers all areas of blood-brain barriers research and reflects the latest developments in neurodegenerative diseases, membrane receptors and transporters, transcytosis regulators, epigenetic and transcriptional regulators, metabolic and nutrition regulation, in vivo and in vitro brain barriers models as well as the role of tight junctions and glycocalyx in blood brain barrier permeability. In addition, signaling pathways implicated in the development of neurological diseases and brain tumors are addressed.. We hope to meet you all in Kraków for this anniversary Blood-Brain Barriers event!. Best ...
Dear Colleagues,. We would like to inform you that the registration and abstract submission for the 20th International Symposium on Signal Transduction at the Blood-Brain Barriers is open till 31st of July and we are looking forward to your registration!. The symposium will be held September 13-15, 2017 in Kraków, Poland.. For more information please see: http://bbb.pan.olsztyn.pl/. The program covers all areas of blood-brain barriers research and reflects the latest developments in neurodegenerative diseases, membrane receptors and transporters, transcytosis regulators, epigenetic and transcriptional regulators, metabolic and nutrition regulation, in vivo and in vitro brain barriers models as well as the role of tight junctions and glycocalyx in blood brain barrier permeability. In addition, signaling pathways implicated in the development of neurological diseases and brain tumors are addressed.. We hope to meet you all in Kraków for this anniversary Blood-Brain Barriers event!. Best ...
The effect of Aβ on BBB integrity has been studied in several cell culture models. Gonzalez-Velasquez et al showed that treatment of cultured human brain endothelial cells with 2.5 to 10 μmol/L Aβ40 triggered the TJ protein ZO-1 to retreat from the plasma membrane, which was accompanied by decreased transendothelial electric resistance.11 Marco and Skaper demonstrated that exposing rat brain endothelial cells to 20 μmol/L Aβ42 triggered ZO-1 and claudin-5 relocation from the plasma membrane, a decrease in occludin expression, and an increase in claudin-1 expression.21 Tai et al demonstrated that Aβ40 activated microtubule-associated protein kinase, which decreased occludin expression and increased permeability in human brain endothelial cell cultures, whereas claudin-5 and ZO-1 remained unchanged.22 Carrano et al analyzed postmortem CAA patient brain slices for TJ protein and observed a loss of occludin, claudin-5, and ZO-1 in brain microvessels.23 We show that hAβ40 decreased rat brain ...
TY - CHAP. T1 - Blood-Brain Barrier Disruption Chemotherapy. AU - McGregor, John M.. AU - Bell, Susan D.. AU - Doolittle, Nancy. AU - Murillo, Tulio P.. AU - Neuwelt, Edward. PY - 2018/4/24. Y1 - 2018/4/24. N2 - The goal of chemotherapy administered in conjunction with blood-brain barrier disruption (BBBD) is maximizing drug delivery to the brain, while preserving the neurocognitive function and minimizing systemic toxicity. In the clinic, BBBD has shown promising results in chemosensitive brain tumors such as the primary central nervous system lymphoma (PCNSL) and offers a new strategy for global delivery of chemotherapy to tumors such as anaplastic oligodendroglioma and central nervous system metastases. Multicenter clinical trials using BBBD are in progress at centers participating in the blood-brain barrier (BBB) Consortium. Current and future clinical studies include delivery of mAbs across the BBB and novel imaging agents to monitor therapeutics.. AB - The goal of chemotherapy administered ...
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Increased permeability of the blood-brain barrier (BBB) is important in neurological disorders. Neuroinflammation is associated with increased BBB breakdown and brain injury. Tumor necrosis factor-alpha (TNF-a) is involved in BBB injury and edema formation through a mechanism involving matrix metalloproteinase (MMP) upregulation. There is emerging evidence indicating that cyclooxygenase (COX) inhibition limits BBB disruption following ischemic stroke and bacterial meningitis, but the mechanisms involved are not known. We used intracerebral injection of TNF-a to study the effect of COX inhibition on TNF-a-induced BBB breakdown, MMP expression/activity and oxidative stress. BBB disruption was evaluated by the uptake of 14C-sucrose into the brain and by magnetic resonance imaging (MRI) utilizing Gd-DTPA as a paramagnetic contrast agent. Using selective inhibitors of each COX isoform, we found that COX-1 activity is more important than COX-2 in BBB opening. TNF-a induced a significant upregulation ...
This unit describes various protocols for the in vivo quantitation of drug permeability across the rodent blood ‐ brain barrier
Reliable human in vitro blood-brain barrier (BBB) models suitable for high-throughput screening are urgently needed in early drug discovery and development for assessing the ability of promising bioactive compounds to overcome the BBB. To establish an improved human in vitro BBB model, we compared four currently available and well characterized immortalized human brain capillary endothelial cell lines, hCMEC/D3, hBMEC, TY10, and BB19, with respect to barrier tightness and paracellular permeability. Co-culture systems using immortalized human astrocytes (SVG-A cell line) and immortalized human pericytes (HBPCT cell line) were designed with the aim of positively influencing barrier tightness. Tight junction (TJ) formation was assessed by transendothelial electrical resistance (TEER) measurements using a conventional epithelial voltohmmeter (EVOM) and an automated CellZscope system which records TEER and cell layer capacitance (CCL) in real-time. Paracellular permeability was assessed using two fluorescent
TY - JOUR. T1 - Chronic inflammatory pain leads to increased blood-brain barrier permeability and tight junction protein alterations. AU - Brooks, Tracy A.. AU - Hawkins, Brian T.. AU - Huber, Jason D.. AU - Egleton, Richard D.. AU - Davis, Thomas P. PY - 2005/8. Y1 - 2005/8. N2 - The blood-brain barrier (BBB) maintains brain homeostasis by limiting entry of substances to the central nervous system through interaction of transmembrane and intracellular proteins that make up endothelial cell tight junctions (TJs). Recently it was shown that the BBB can be modulated by disease pathologies including inflammatory pain. This study examined the effects of chronic inflammatory pain on the functional and molecular integrity of the BBB. Inflammatory pain was induced by injection of complete Freunds adjuvant (CFA) into the right plantar hindpaw in female Sprague-Dawley rats under halothane anesthesia; control animals were injected with saline. Edema and hyperalgesia were assessed by plethysmography and ...
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Modelling of the blood-brain barrier transport of morphine-3-glucuronidestudied using microdialysis in the rat: involvement ofprobenecid-sensitive transport. ...
The purpose of this study was to investigate whether a relationship exists between alterations of the blood-brain barrier (BBB) and the survival time of rats exposed to supralethal irradiation. BBB alterations were produced by injection of glycerol, mercuric chloride, or by lymphatic cervical blockade. Animals were subsequently exposed to a supralethal dose of radiation, and the survival times of various groups were compared. The production of BBB alterations prior to irradiation did not influence the survival time of rats after exposure to supralethal doses of radiation suggesting that BBB damage may bear no direct relationship to the survival time after radiation injury. (Author)
Blood-brain barrier (BBB) leakage plays a key role in cerebral ischemia-reperfusion injury. It is quite necessary to further explore the characteristic and mechanism of BBB leakage during stroke. We induced a focal cerebral ischemia model by transient middle cerebral artery occlusion in male rats for defining the time course of BBB permeability within 120 h following reperfusion and evaluate the specific role of tight junction (TJ) associated proteins claudin-5, occludin, and ZO-1 as well as protein kinase C delta (PKCδ) pathway in BBB leakage induced by reperfusion injury. We verified a bimodal increase in the permeability of the BBB following focal ischemia by Evans blue assay. Two peaks of BBB permeability appeared at 3 h and 72 h of reperfusion after 2 h focal ischemia, respectively. The leak at the endothelial cell was represented at the level of transmission electron microscopy. TTC staining results showed increased infarct size with time after cerebral ischemia reperfusion. The mRNA and ...
Although the mechanisms of action of antipsychotics (APs) on neuronal function are well understood, very little is known about their effects on cells of the blood-brain barrier (BBB); one function of which is to limit the access of these amphiphilic compounds to the central nervous system. To address this question we have investigated the cytological and functional effects of four APs: chlorpromazine (CLP), haloperidol (HAL), risperidone (RIS) and clozapine (CLZ), at concentrations typical of high therapeutic dosage on a human brain microvascular endothelial cell (HBMEC) model of the BBB. At ~10 µM all four APs impaired the ability of HBMECs to reduce MTT which was followed by decreased Trypan blue exclusion and increased Lactate dehydrogenase release. These effects were associated with oxidative stress which was partly reversed by incubation in 10 mM glutathione. At their EC50 concentrations for MTT reduction, all four APs disrupted cellular ultrastructure and morphology. HAL, CPZ and CLZ ...
The blood-brain barrier (BBB) plays an important role in brain homeostasis. Hypoxia/ischemia constitutes an important stress factor involved in several neurological disorders by inducing the...
An intact blood-brain barrier and normal production, circulation, and absorption of cerebrospinal fluid are critical for normal brain function. Minor disruptions of barrier function are without clinical consequences. Major disruptions accompany most significant acute brain injuries. The anatomic location of the blood-brain barrier is the endothelial cells of arterioles, capillaries, veins, and the epithelial cell surface of the choroid plexus. However, endothelial cells require the presence of glial cells to maintain barrier function. During cardiopulmonary bypass, several factors may result in a temporary disruption of the barrier; the most important are systemic inflammatory response and focal ischemia due to emboli. Lacking a lymphatic system, the brain depends on the circulation of cerebrospinal fluid to remove the products of metabolism, and the circulation of cerebrospinal fluid depends on a vascular systolic pulse wave to drive this fluid antegrade along the brain paravascular spaces. Although it
Blood-brain barrier (BBB) disruption and neuroinflammation are considered key mechanisms of pathogenic Escherichia coli invasion of the brain. However, the specific molecules involved in meningitic E. coli-induced BBB breakdown and neuroinflammatory response remain unclear. Our previous RNA-sequencing data from human brain microvascular endothelial cells (hBMECs) revealed two important host factors: platelet-derived growth factor-B (PDGF-B) and intercellular adhesion molecule-1 (ICAM-1), which were significantly upregulated in hBMECs after meningitic E. coli infection. Whether and how PDGF-B and ICAM-1 contribute to the development of E. coli meningitis are still unclear. The western blot, real-time PCR, enzyme-linked immunosorbent assay, immunohistochemistry, and immunofluorescence were applied to verify the significant induction of PDGF-B and ICAM-1 by meningitic E. coli in vivo and in vitro. Evans blue assay and electric cell-substrate impedance sensing assay were combined to identify the effects of
Age-related ultrastructural changes of the basement membrane in the mouse blood-brain barrier has been published in the Journal of Cellular and Molecular
Age-related ultrastructural changes of the basement membrane in the mouse blood-brain barrier has been published in the Journal of Cellular and Molecular
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The blood-brain barrier is a physical and physiological barrier that protects the brain from toxic substances within the bloodstream and helps maintain brain homeostasis. It also represents the main obstacle in the treatment of many diseases of the central nervous system. Among the different approaches employed to overcome this barrier, the use of nanoparticles as a tool to enhance delivery of therapeutic molecules to the brain is particularly promising. There is special interest in the use of magnetic nanoparticles, as their physical characteristics endow them with additional potentially useful properties. Following systemic administration, a magnetic field applied externally can mediate the capacity of magnetic nanoparticles to permeate the blood-brain barrier. Meanwhile, thermal energy released by magnetic nanoparticles under the influence of radiofrequency radiation can modulate blood-brain barrier integrity, increasing its permeability. In this review, we present the strategies that use magnetic
Delayed administration of vascular endothelial growth factor (VEGF) promotes functional recovery after focal cerebral ischemia. However, early intravenous injection of VEGF increases blood-brain barrier (BBB) leakage, hemorrhagic transformation and infarct volume whereas its application to cortical surface is neuroprotective. We have investigated whether or not early intracerebroventricular administration of VEGF could replicate the neuroprotective effect observed with topical application and the mechanism of action of this protection. Mice were subjected to 90 mins middle cerebral artery (MCA) occlusion and 24h of reperfusion. Vascular endothelial growth factor (8ng, intracerebroventricular) was administered 1 or 3h after reperfusion. Compared with the vehicle-treated (intracerebroventricular) group, VEGF decreased the infarct volume along with BBB leakage in both treatment groups. Neurologic disability scores improved in parallel to the changes in infarct volume. Independently of the decrease ...
Cardiac arrest and resuscitation in immature piglets result in a delayed increase in blood-brain barrier permeability. We tested the hypothesis that pretreatment with oxygen radical scavengers reduces postischemic permeability.. Permeability was assessed by measuring the plasma-to-brain transfer coefficient of the small amino acid, alpha-aminoisobutyric acid, in 2- to 3-week-old anesthetized piglets. Three groups were studied: (1) a nonischemic time control group (n = 5), (2) an ischemia group (n = 8) pretreated with 5 mL of polyethylene glycol vehicle, and (3) an ischemia group (n = 8) pretreated with polyethylene glycol conjugated to superoxide dismutase (10,000 U/kg) and to catalase (20,000 U/kg). The ischemia protocol consisted of 8 minutes of ventricular fibrillation, 6 minutes of cardiopulmonary resuscitation, defibrillation, and 4 hours of spontaneous circulation.. The mean +/- SEM of the transfer coefficient of alpha-aminoisobutyric acid in cerebrum was (in microL/g per minute): 1.54 +/- ...
Video articles in JoVE about animals domestic include Assessing Transmissible Spongiform Encephalopathy Species Barriers with an In Vitro Prion Protein Conversion Assay, Development of a Colloidal Gold-based Immunochromatographic Test Strip for Detection of Cetacean Myoglobin, Fecal Glucocorticoid Analysis: Non-invasive Adrenal Monitoring in Equids, Improved Method for the Establishment of an In Vitro Blood-Brain Barrier Model Based on Porcine Brain Endothelial Cells, Magnetic Stirrer Method for the Detection of Trichinella Larvae in Muscle Samples, Thermal Imaging to Study Stress Non-invasively in Unrestrained Birds, Use of a Piglet Model for the Study of Anesthetic-induced Developmental Neurotoxicity (AIDN): A Translational Neuroscience Approach, Transabdominal Ultrasound for Pregnancy Diagnosis in Reeves Muntjac Deer, Spotting Cheetahs: Identifying Individuals by Their Footprints, The Bovine Lung in Biomedical Research: Visually Guided Bronchoscopy, Intrabronchial Inoculation and
phdthesis{2056153, abstract = {Several endogenous active peptides exist in the central nervous system (CNS), but the CNS drug development is hampered by the presence of the blood-brain barrier (BBB). The evaluation, modeling and understanding of the transport mechanisms at the BBB is very important for the development and optimization of potential CNS peptide drugs. Which techniques are used to quantitatively describe the BBB transport properties? Due to the multi-disciplinary complexity of the BBB research, several methodologies, each resulting in a specific parameter, are reported. Therefore, a coherent overview of the BBB-responses was described and a comprehensive database (Brainpeps{\textregistered}) constructed to collect the dispersed literature data. Chromatographic behavior of peptides on fused-core stationary phases? A representative peptide set was obtained via hierarchic clustering based on their structure properties. The chromatographic peptide interactions on the fused-core systems ...
Video articles in JoVE about membrane potentials include A Computerized Test Battery to Study Pharmacodynamic Effects on the Central Nervous System of Cholinergic Drugs in Early Phase Drug Development, Electroretinogram Analysis of the Visual Response in Zebrafish Larvae, Implementation of a Permeable Membrane Insert-based Infection System to Study the Effects of Secreted Bacterial Toxins on Mammalian Host Cells, Improved Method for the Establishment of an In Vitro Blood-Brain Barrier Model Based on Porcine Brain Endothelial Cells, A Microfluidic System with Surface Patterning for Investigating Cavitation Bubble(s)-Cell Interaction and the Resultant Bioeffects at the Single-cell Level, Isolation of Type I and Type II Pericytes from Mouse Skeletal Muscles, Phase Behavior of Charged Vesicles Under Symmetric and Asymmetric Solution Conditions Monitored with Fluorescence Microscopy, From Fast Fluorescence Imaging to Molecular Diffusion Law on Live Cell Membranes in a Commercial Microscope,
A high-functioning blood brain barrier is obviously crucial to a high-functioning mind. Yet defense of the brain from inflammation and peripheral mayhem is not always effective. Molecules like alcohol easily pay off the guards and make the brain a pickled mess; it is no surprise when toxic substances such as ethanol and drugs cause problems in thinking and memory.. Yet domestic disturbances can also impact blood brain barrier function and thus brain function. For instance metabolic imbalances in glucose-both hyper- and hypoglycemia-are risk factors. Metabolic stress leads to immune dysfunction which may be one mechanism of action. (read Metabolic Syndrome and the Immunological Affair with the Blood-Brain Barrier in Frontiers in Immunology for an excellent instruction on the complex structure and function of blood-brain barrier systems).. Researchers are beginning to explore the effect of microbes.. They recently discovered that germ-free mice were different than control mice in this ...
The blood brain barrier is a network of tight junctions of endothelial cells in the central nervous system vessels. The cells are polarized into luminal (blood-facing) and abluminal (brain-facing) plasma membrane domains. These protective membranes serve to allow substances to cross into and out of the brain selectively. In a newborn, it takes approximately six weeks for the blood brain barrier to become formed.. Within the blood brain barrier there are circumventricular organs which include: a.) the Pineal body which secretes melatonin, associated with the normal twenty-four hour sleep/wake cycle; b.) the posterior Pituitary which releases neurohormones like oxytoxin (responsible for bonding) and vasopressin (which plays a key role in the regulation of water, glucose, and salts in the blood; c.) the Subfornical organ which is important for regulation of body fluids and; d.) the Vascular organ, a chemosensory area that detects peptides. Each of these organs is sensitive to toxicity. If any of ...
Ischemic brain injury disrupts the blood-brain barrier (BBB) and then triggers a cascade of events, leading to edema formation, secondary brain injury and poor neurological outcomes. Recently, we have shown that docosahexaenoic acid (DHA) improves functional and histological outcomes following experimental stroke. However, little is known about the effect of DHA on BBB dysfunction after cerebral ischemia-reperfusion injury. The present study was designed to determine whether DHA protects against BBB disruption after focal cerebral ischemia in rats. Physiologically-controlled SD rats received 2 h middle cerebral artery occlusion (MCAo). DHA (5 mg/kg) or vehicle (saline) was administered I.V. at 3 h after onset of MCAo. Fluorometric quantitation of Evans Blue dye (EB) was performed in eight brain regions at 6 h, 24 h or 72 h after MCAo. Fluorescein isothiocynate (FITC) - dextran leakage and histopathology was evaluated on day 3 after stroke. Physiological variables were stable and showed no significant
St. Marys College student Randy Larsen IV 19 spent the summer interning at the Womens Malignancies Branch of the National Cancer Institute. Under Senior Investigator Patricia Steeg, the lab focused on the mechanisms of how breast cancer metastasizes into the brain.. Larsens day-to-day mentor was researcher Lin Xiao. "Working with Dr. Xiao, my project focused on validating the use of induced pluripotent stem cells to create a more functionally accurate in vitro blood-brain barrier model," said Larsen. "In laymans terms, we cultured stem cells into brain cells - endothelial cells specifically - and found that when we used those new induced endothelial cells, our model behaved more like the in vivo brain compared to many currently used in vitro models.". "I had an amazing time working under Dr. Xiao and Dr. Steeg," said Larsen. "They were incredibly supportive, no matter how frustrating and time-consuming parts of my project were. Besides sharpening my lab skills, it was great to see what the ...
Hypoxic Stress Induced by Hydralazine Leads to a Loss of Blood-Brain Barrier Integrity and an Increase in Efflux Transporter Activity. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
In order to meet the high metabolic needs of the neurons "behind" the barrier in spite of its restrictive capacity, specific transport systems are selectively expressed in the CNS microvascular endothelial cells, which mediate the directed transport of nutrients from the blood into the CNS or the removal of toxic metabolites out of the CNS. Recent years have dramatically advanced our knowledge about the growth factors and their receptors specifically acting on the developing vascular endothelium including the CNS vasculature. Sci. Am. 255, 74-83. Janzer, R. , Raff, M. C. 1987, Astrocytes induce blood-brain barrier properties in endothelial cells. Nature 325, 253-257. Nag, S. 2003, The Blood-Brain Barrier, Humana Press, Totowa. , Helmchen, F. 2005, Resting microglial cells are highly dynamic surveillants of brain parenchyma in vivo. Science 308, 1314-1318. Pardrige, W. M. 1993, The Blood-Brain Barrier: Cellular and Molecular Biology, Raven Press, New York. Paulson, O. , Moos, T. 1999, Blood-Brain ...
The role of nitric oxide (NO) in blood-brain barrier (BBB) or blood-spinal cord barriers (BSCB) disruption following central nervous system (CNS) injuries is not known in details. New data from our laboratory show that inhibition of neuronal nitric oxide synthase (NOS) expression by drugs or antibodies attenuate BBB and BSCB breakdown in CNS trauma or hyperthermia leading to neuroprotection. This review critically examines the role of NO in microvascular permeability disturbances following CNS injuries and other related neurological disorders. It appears that NO plays an important role in the breakdown of the BBB and BSCB function in CNS diseases. This indicates that NOS inhibitors have potential therapeutic value in CNS injuries or neurodegeneration in the near future.. ...
Date: November 19, 2014 Source: Karolinska Institutet Summary: Our natural gut-residing microbes can influence the integrity of the blood-brain barrier, which protects the brain from harmful substances in the blood, a new study in mice shows. The blood-brain barrier is a highly selective barrier that prevents unwanted molecules and cells from entering the brain from…
Recent studies have shown that the blood-brain barrier is severely altered in epilepsy and that barrier dysfunction affects neuronal function and leads to seizures (Marchi et al., 2007a,b; Rigau et al., 2007; van Vliet et al., 2007; Tomkins et al., 2008; Kastanauskaite et al., 2009; Alonso-Nanclares and DeFelipe, 2014). One critical element of barrier dysfunction is barrier leakage, which was observed in animal seizure and epilepsy models as well as in epilepsy patients (Nitsch and Klatzo, 1983; Mihály and Bozóky, 1984; Cornford and Oldendorf, 1986; Horowitz et al., 1992; Padou et al., 1995). Our data from the present study are consistent with these observations. Several studies showed that blood-brain barrier leakage in epilepsy was restricted to anatomically specific brain regions and that these brain regions are often implicated in the development and propagation of seizures (Nitsch and Klatzo, 1983; Cornford et al., 1998). This suggests a connection between barrier leakage and seizures. ...
When ultrasound bursts are combined with a circulating microbubble agent, a temporary disruption in the blood-brain barrier (BBB) is induced that lasts for seve...
Objective: The normal blood brain barrier (BBB) is composed of tight junctions between endothelial cells and surrounding astrocyte foot processes. Breakdown of the physiological astrocyte-endothelial cell relationship occurs in adult metastatic and primary brain tumors. However, the astrocyte-endothelial cell relationship has not been studied in pediatric tumors. Materials and Methods: Utilizing specimens from cases of pilocytic astrocytoma (n = 5), medulloblastoma (n = 5), and low-grade diffuse astrocytoma (n = 1), immunofluorescence were performed using primary antibodies against CD31, glial fibrillary acidic protein (GFAP), and aquaporin 4 (AQ4). Clinical, magnetic resonance imaging, operative, and histopathological findings were analyzed. Results: Strongly-enhancing areas of medulloblastoma exhibited complete BBB breakdown with sparse GFAP and AQ4 staining around CD31-positive vessels. Moderately enhancing regions of pilocytic astrocytomas exhibited regions of intact BBB and vasculature ...
TY - JOUR. T1 - Biocompatible Red Fluorescent Organic Nanoparticles with Tunable Size and Aggregation-Induced Emission for Evaluation of Blood-Brain Barrier Damage. AU - Cai, Xiaolei. AU - Bandla, Aishwarya. AU - Mao, Duo. AU - Feng, Guangxue. AU - Qin, Wei. AU - Liao, Lun De. AU - Thakor, Nitish V. AU - Tang, Ben Zhong. AU - Liu, Bin. PY - 2016/10/19. Y1 - 2016/10/19. KW - aggregation-induced emission. KW - blood-brain barrier damage. KW - nanoparticles. KW - photothrombotic ischemia. KW - stroke. UR - http://www.scopus.com/inward/record.url?scp=84992109013&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=84992109013&partnerID=8YFLogxK. U2 - 10.1002/adma.201601191. DO - 10.1002/adma.201601191. M3 - Article. C2 - 27511643. AN - SCOPUS:84992109013. VL - 28. SP - 8760. EP - 8765. JO - Advanced Materials. JF - Advanced Materials. SN - 0935-9648. IS - 39. ER - ...