Blood-Retinal Barrier: A specialized transport barrier, in the EYE, formed by the retinal pigment EPITHELIUM, and the ENDOTHELIUM of the BLOOD VESSELS of the RETINA. TIGHT JUNCTIONS joining adjacent cells keep the barrier between cells continuous.Microfluidic Analytical Techniques: Methods utilizing the principles of MICROFLUIDICS for sample handling, reagent mixing, and separation and detection of specific components in fluids.Microfluidics: The study of fluid channels and chambers of tiny dimensions of tens to hundreds of micrometers and volumes of nanoliters or picoliters. This is of interest in biological MICROCIRCULATION and used in MICROCHEMISTRY and INVESTIGATIVE TECHNIQUES.Dimethylpolysiloxanes: Silicone polymers which consist of silicon atoms substituted with methyl groups and linked by oxygen atoms. They comprise a series of biocompatible materials used as liquids, gels or solids; as film for artificial membranes, gels for implants, and liquids for drug vehicles; and as antifoaming agents.Retinal Vessels: The blood vessels which supply and drain the RETINA.Leukostasis: Abnormal intravascular leukocyte aggregation and clumping often seen in leukemia patients. The brain and lungs are the two most commonly affected organs. This acute syndrome requires aggressive cytoreductive modalities including chemotherapy and/or leukophoresis. It is differentiated from LEUKEMIC INFILTRATION which is a neoplastic process where leukemic cells invade organs.Capillary Permeability: The property of blood capillary ENDOTHELIUM that allows for the selective exchange of substances between the blood and surrounding tissues and through membranous barriers such as the BLOOD-AIR BARRIER; BLOOD-AQUEOUS BARRIER; BLOOD-BRAIN BARRIER; BLOOD-NERVE BARRIER; BLOOD-RETINAL BARRIER; and BLOOD-TESTIS BARRIER. Small lipid-soluble molecules such as carbon dioxide and oxygen move freely by diffusion. Water and water-soluble molecules cannot pass through the endothelial walls and are dependent on microscopic pores. These pores show narrow areas (TIGHT JUNCTIONS) which may limit large molecule movement.Pigment Epithelium of Eye: The layer of pigment-containing epithelial cells in the RETINA; the CILIARY BODY; and the IRIS in the eye.Encyclopedias as Topic: Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)Diabetic Retinopathy: Disease of the RETINA as a complication of DIABETES MELLITUS. It is characterized by the progressive microvascular complications, such as ANEURYSM, interretinal EDEMA, and intraocular PATHOLOGIC NEOVASCULARIZATION.Blood-Aqueous Barrier: The selectively permeable barrier, in the EYE, formed by the nonpigmented layer of the EPITHELIUM of the CILIARY BODY, and the ENDOTHELIUM of the BLOOD VESSELS of the IRIS. TIGHT JUNCTIONS joining adjacent cells keep the barrier between cells continuous.Retina: The ten-layered nervous tissue membrane of the eye. It is continuous with the OPTIC NERVE and receives images of external objects and transmits visual impulses to the brain. Its outer surface is in contact with the CHOROID and the inner surface with the VITREOUS BODY. The outer-most layer is pigmented, whereas the inner nine layers are transparent.Cellophane: A generic name for film produced from wood pulp by the viscose process. It is a thin, transparent sheeting of regenerated cellulose, moisture-proof and sometimes dyed, and used chiefly as food wrapping or as bags for dialysis. (Grant & Hackh's Chemical Dictionary, 5th ed & McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)Crisscross Heart: A developmental malformation of the heart characterized by a twisted but not defective atrioventicular connection. The abnormal rotation of the ventricular mass around its long axis results in the crossing of the inflow streams of the two ventricles. Other features include hypoplasia of the TRICUSPID VALVE and RIGHT VENTRICLE.Microtechnology: Manufacturing technology for making microscopic devices in the micrometer range (typically 1-100 micrometers), such as integrated circuits or MEMS. The process usually involves replication and parallel fabrication of hundreds or millions of identical structures using various thin film deposition techniques and carried out in environmentally-controlled clean rooms.Hammer Toe Syndrome: A condition characterized by a series of interrelated digital symptoms and joint changes of the lesser digits and METATARSOPHALANGEAL JOINTS of the FOOT. The syndrome can include some or all of the following conditions: hammer toe, claw toe, mallet toe, overlapping fifth toe, curly toe, EXOSTOSIS; HYPEROSTOSIS; interdigital heloma, or contracted toe.Membranes, Artificial: Artificially produced membranes, such as semipermeable membranes used in artificial kidney dialysis (RENAL DIALYSIS), monomolecular and bimolecular membranes used as models to simulate biological CELL MEMBRANES. These membranes are also used in the process of GUIDED TISSUE REGENERATION.Toxoplasma: A genus of protozoa parasitic to birds and mammals. T. gondii is one of the most common infectious pathogenic animal parasites of man.Toxoplasmosis, Animal: Acquired infection of non-human animals by organisms of the genus TOXOPLASMA.Toxoplasmosis, Ocular: Infection caused by the protozoan parasite TOXOPLASMA in which there is extensive connective tissue proliferation, the retina surrounding the lesions remains normal, and the ocular media remain clear. Chorioretinitis may be associated with all forms of toxoplasmosis, but is usually a late sequel of congenital toxoplasmosis. The severe ocular lesions in infants may lead to blindness.Toxoplasmosis: The acquired form of infection by Toxoplasma gondii in animals and man.Tight Junctions: Cell-cell junctions that seal adjacent epithelial cells together, preventing the passage of most dissolved molecules from one side of the epithelial sheet to the other. (Alberts et al., Molecular Biology of the Cell, 2nd ed, p22)Intravitreal Injections: The administration of substances into the VITREOUS BODY of the eye with a hypodermic syringe.Tomography, Optical Coherence: An imaging method using LASERS that is used for mapping subsurface structure. When a reflective site in the sample is at the same optical path length (coherence) as the reference mirror, the detector observes interference fringes.Vitreous Body: The transparent, semigelatinous substance that fills the cavity behind the CRYSTALLINE LENS of the EYE and in front of the RETINA. It is contained in a thin hyaloid membrane and forms about four fifths of the optic globe.Fluorescein Angiography: Visualization of a vascular system after intravenous injection of a fluorescein solution. The images may be photographed or televised. It is used especially in studying the retinal and uveal vasculature.Retinal Vein Occlusion: Blockage of the RETINAL VEIN. Those at high risk for this condition include patients with HYPERTENSION; DIABETES MELLITUS; ATHEROSCLEROSIS; and other CARDIOVASCULAR DISEASES.Hypoxia-Ischemia, Brain: A disorder characterized by a reduction of oxygen in the blood combined with reduced blood flow (ISCHEMIA) to the brain from a localized obstruction of a cerebral artery or from systemic hypoperfusion. Prolonged hypoxia-ischemia is associated with ISCHEMIC ATTACK, TRANSIENT; BRAIN INFARCTION; BRAIN EDEMA; COMA; and other conditions.Retinal Vein: Central retinal vein and its tributaries. It runs a short course within the optic nerve and then leaves and empties into the superior ophthalmic vein or cavernous sinus.Vascular Endothelial Growth Factor A: The original member of the family of endothelial cell growth factors referred to as VASCULAR ENDOTHELIAL GROWTH FACTORS. Vascular endothelial growth factor-A was originally isolated from tumor cells and referred to as "tumor angiogenesis factor" and "vascular permeability factor". Although expressed at high levels in certain tumor-derived cells it is produced by a wide variety of cell types. In addition to stimulating vascular growth and vascular permeability it may play a role in stimulating VASODILATION via NITRIC OXIDE-dependent pathways. Alternative splicing of the mRNA for vascular endothelial growth factor A results in several isoforms of the protein being produced.Animal Experimentation: The use of animals as investigational subjects.Macular Edema: Fluid accumulation in the outer layer of the MACULA LUTEA that results from intraocular or systemic insults. It may develop in a diffuse pattern where the macula appears thickened or it may acquire the characteristic petaloid appearance referred to as cystoid macular edema. Although macular edema may be associated with various underlying conditions, it is most commonly seen following intraocular surgery, venous occlusive disease, DIABETIC RETINOPATHY, and posterior segment inflammatory disease. (From Survey of Ophthalmology 2004; 49(5) 470-90)Brain Edema: Increased intracellular or extracellular fluid in brain tissue. Cytotoxic brain edema (swelling due to increased intracellular fluid) is indicative of a disturbance in cell metabolism, and is commonly associated with hypoxic or ischemic injuries (see HYPOXIA, BRAIN). An increase in extracellular fluid may be caused by increased brain capillary permeability (vasogenic edema), an osmotic gradient, local blockages in interstitial fluid pathways, or by obstruction of CSF flow (e.g., obstructive HYDROCEPHALUS). (From Childs Nerv Syst 1992 Sep; 8(6):301-6)Blood-Brain Barrier: Specialized non-fenestrated tightly-joined ENDOTHELIAL CELLS with TIGHT JUNCTIONS that form a transport barrier for certain substances between the cerebral capillaries and the BRAIN tissue.Proteome: The protein complement of an organism coded for by its genome.Horse Diseases: Diseases of domestic and wild horses of the species Equus caballus.Retinal Pigment Epithelium: The single layer of pigment-containing epithelial cells in the RETINA, situated closely to the tips (outer segments) of the RETINAL PHOTORECEPTOR CELLS. These epithelial cells are macroglia that perform essential functions for the photoreceptor cells, such as in nutrient transport, phagocytosis of the shed photoreceptor membranes, and ensuring retinal attachment.Mass Spectrometry: An analytical method used in determining the identity of a chemical based on its mass using mass analyzers/mass spectrometers.Horses: Large, hoofed mammals of the family EQUIDAE. Horses are active day and night with most of the day spent seeking and consuming food. Feeding peaks occur in the early morning and late afternoon, and there are several daily periods of rest.Isocitrate Dehydrogenase: An enzyme of the oxidoreductase class that catalyzes the conversion of isocitrate and NAD+ to yield 2-ketoglutarate, carbon dioxide, and NADH. It occurs in cell mitochondria. The enzyme requires Mg2+, Mn2+; it is activated by ADP, citrate, and Ca2+, and inhibited by NADH, NADPH, and ATP. The reaction is the key rate-limiting step of the citric acid (tricarboxylic) cycle. (From Dorland, 27th ed) (The NADP+ enzyme is EC 1.1.1.42.) EC 1.1.1.41.Mutation: Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.United StatesPoint Mutation: A mutation caused by the substitution of one nucleotide for another. This results in the DNA molecule having a change in a single base pair.IsocitratesMutation, Missense: A mutation in which a codon is mutated to one directing the incorporation of a different amino acid. This substitution may result in an inactive or unstable product. (From A Dictionary of Genetics, King & Stansfield, 5th ed)Cell Line, Tumor: A cell line derived from cultured tumor cells.Heart: The hollow, muscular organ that maintains the circulation of the blood.Cicatrix: The fibrous tissue that replaces normal tissue during the process of WOUND HEALING.Heart Rate: The number of times the HEART VENTRICLES contract per unit of time, usually per minute.Chlorthalidone: A benzenesulfonamide-phthalimidine that tautomerizes to a BENZOPHENONES form. It is considered a thiazide-like diuretic.Myocardial Infarction: NECROSIS of the MYOCARDIUM caused by an obstruction of the blood supply to the heart (CORONARY CIRCULATION).Schools: Educational institutions.Endothelial Cells: Highly specialized EPITHELIAL CELLS that line the HEART; BLOOD VESSELS; and lymph vessels, forming the ENDOTHELIUM. They are polygonal in shape and joined together by TIGHT JUNCTIONS. The tight junctions allow for variable permeability to specific macromolecules that are transported across the endothelial layer.

Immune responses limit adenovirally mediated gene expression in the adult mouse eye. (1/301)

In order to investigate the immunological consequences of gene transfer to the eye using viral vectors, adenovirus carrying a lacZ reporter gene (AV.LacZ) was injected either subretinally, subconjunctivally or into the anterior chamber of three groups of adult mice: immunocompetent or transiently immunosuppressed BALB/c mice and congenic immunodeficient nude mice. Adenovirally mediated lacZ expression persisted for approximately 3 weeks following injection of the vector into the anterior chamber, retina or extra ocular tissues of the conjuctiva of BALB/c mice. It appears that T cell-mediated immune responses limit the duration of AV-mediated ocular gene expression in adult mice since lacZ gene expression was detected for at least 15 weeks in T cell-deficient BALB/c nude mice, although the level of transgene expression decreased with time. Since intra-ocular AV-mediated gene expression was not significantly longer than extra-ocular expression, it appears that the eye is not normally immune-privileged with respect to viral vectors. Inflammatory cells were detected in the vitreous after anterior chamber injection and in the retina after subretinal injection of adenovirus. The presence of both CD4+ and CD8+ T cells was established by immunophenotyping. Reinjection of BALB/c mice resulted in rapid decline in reporter gene expression, but successful readministration was possible in the case of immunodeficient nude mice. However, after transient depletion of T cells, achieved by intraperitoneal injection of both CD8- and CD4-specific antibodies, the duration of expression in BALB/c mice was longer in the eye (at least 12 weeks, again with decrease in level over time), than in extra-ocular tissues (8 weeks) provided the animal was not reinjected with virus raising the possibility of partial ocular immune-privilege after transient immunosuppression.  (+info)

Effects of acetazolamide on passive and active transport of fluorescein across the normal BRB. (2/301)

PURPOSE: To investigate the effect of the carbonic anhydrase inhibitor acetazolamide (AZM) on passive permeability and active transport of fluorescein across the blood-retina barrier in healthy subjects. The study may have implications for the understanding of the edema-reducing effect of AZM. METHODS: The effect of AZM on the blood-retina barrier function was assessed by differential vitreous spectrofluorometry using fluorescein as a tracer. The study included fourteen healthy subjects in a randomized double-masked crossover trial with 3 days' treatment with AZM (500 mg/d) and placebo, respectively. The two examinations were separated by at least 1 week. Fluorescein concentration was determined separately from its metabolite fluorescein glucuronide. The passive permeability of fluorescein was determined by computerized modeling and curve-fitting to the preretinal curve and the plasma concentration curve obtained at 30 to 60 minutes after the injection of fluorescein. The unidirectional permeability due to outward active transport from vitreous to blood was estimated from the preretinal gradient and the plasma concentration at 7 to 10 hours after injection. RESULTS: Treatment with AZM was associated with significant increases in passive permeability and unidirectional permeability of fluorescein. For the passive permeability the increase was on average 0.3+/-0.4 nm/s (mean+/-SD; range, -0.8-1.0 nm/s), and for the unidirectional permeability the increase was on average 7.4 nm/s+/-7.0 (mean+/-SD; range, -3.3-19.0 nm/s). CONCLUSIONS: Acetazolamide caused an increase in passive permeability. Unidirectional permeability was increased by AZM, indicating a stimulation of the outward active transport of fluorescein. It has been proposed that the edema-reducing effect of AZM is due to stimulated ion and fluid removal from the retina to the choroid. The results of this study are consistent with AZM affecting the blood-retina barrier with stimulation of at least one ion transport mechanism.  (+info)

Remodeling of retinal capillaries in the diabetic hypertensive rat. (3/301)

PURPOSE: To document the effect of sustained systemic hypertension on the integrity and ultrastructural morphology of retinal capillaries in diabetic and nondiabetic rats. METHODS: Normotensive (strain Wistar-Kyoto; WKY) and genetically hypertensive (spontaneously hypertensive; SHR) rats were rendered diabetic by intravenous streptozotocin injection. At 20 weeks of diabetes, endothelial cells, pericytes, and extracellular matrix were evaluated by ultrastructural morphometry. Serum albumin was localized by immunofluorescence microscopy. RESULTS: The endothelial cell layer was markedly thinner in the diabetic normotensive animals. The number of intercellular junctions was reduced in both the nondiabetic and diabetic hypertensive group but less so in the diabetic normotensive group. No significant endothelial cell loss was noted in either of the experimental groups, whereas the number of pericytes and the number of their cytoplasmic processes were reduced in diabetic and hypertensive animals. Significant thickening of the basement membrane and increased permeability to serum albumin were observed in diabetic and hypertensive rats and were strongly enhanced in the combined diseases. CONCLUSIONS: Endothelial thinning and shape changes from an elaborate to a simpler form as well as rounding up of the pericytes and loosening of their vascular sheaths indicate remodeling of the vascular wall during chronic diabetes and sustained hypertension, before a characteristic vasculopathy becomes manifest. The combination of diabetes and hypertension enhances these features, as well as basement membrane thickening and breakdown of the blood-retinal barrier.  (+info)

Physiology of rat retinal pericytes: modulation of ion channel activity by serum-derived molecules. (4/301)

1. Pericytes, which are contractile cells located on the outer wall of microvessels, are thought to be particularly important in the retina where the ratio of these cells to vascular endothelial cells is the highest of any tissue. Retinal pericytes are of interest since they may regulate capillary blood flow and because their selective loss is an early event in diabetic retinopathy, which is a common sight-threatening disorder associated with dysfunction of the blood-retinal barrier. 2. Although a breakdown in the vascular endothelial barrier is a frequent pathophysiological event, knowledge of the effects of blood-derived molecules on pericyte function is limited. Based on the premise that ion channels play a vital role in cellular function, we examined the effect of serum on the ionic currents of retinal pericytes. To do this, we used the perforated-patch configuration of the patch-clamp technique to monitor the whole-cell currents of pericytes located on freshly isolated rat retinal microvessels. 3. Exposure to serum reversibly activated inward and outward currents in virtually all of the sampled retinal pericytes. Two types of sustained conductances were induced by serum. These were a calcium-permeable non-specific cation (NSC) current and a voltage-dependent potassium current. In addition, exposure to serum increased the activity of chloride channels which caused transient depolarizing currents. 4. Associated with the activation of these conductances, the membrane potential showed a sustained decrease of 10 +/- 2 mV from -56 mV to -46 mV and, also, transient depolarizations to near -30 mV. The serum-induced depolarizations can activate the voltage-gated calcium channels expressed by the retinal pericytes. 5. Calcium-permeable NSC channels appear to play a critical role in the response of pericytes to serum-derived molecules. Consistent with this, activation of the chloride and potassium channels was sensitive to SK&F 96365, which is a blocker of NSC channels. In addition, chloride and potassium channel activation was dependent on extracellular calcium. 6. The effects of serum on the activity of channels in retinal pericytes were qualitatively mimicked by insulin-like growth factor-1 (IGF-1), which is a normal constituent of the blood. 7. There are significant differences in the effects of serum on retinal pericytes compared with vascular smooth muscle cells. Serum activated sustained conductances in retinal pericytes but not in the vascular smooth muscle cells. This suggests a fundamental difference in the mechanisms by which serum-derived molecules affect these two types of cells. 8. We conclude that serum-derived molecules, such as IGF-1, can activate several types of ion channels in retinal pericytes. These changes in channel activity are likely to influence pericyte function at sites of a breakdown in the blood-retinal barrier.  (+info)

Differential expression of endothelial beta-catenin and plakoglobin during development and maturation of the blood-brain and blood-retina barrier in the chicken. (5/301)

The development of the blood-brain barrier depends upon the formation of a closely regulated system of adherens and tight junctions. A prerequisite for a functional junction system is the linkage of transmembrane adhesion receptors (cadherins) to the cytoskeleton via catenins. The localization of specific catenins at the adherens junction correlates with the stability of interendothelial contacts in vitro, but in vivo data are lacking thus far. Investigating brain angiogenesis in the chicken, we demonstrated that beta-catenin, but not plakoglobin, initially codistributed with N-cadherin at the ablumenal endothelial membrane at contact sites to perivascular cells, from where both antigens disappeared during blood-brain barrier maturation. In contrast, plakoglobin was most prominent at the interendothelial junction where only small amounts of beta-catenin were present. Western-blot analysis revealed a stronger developmental decrease of beta-catenin than plakoglobin, whereas N-cadherin was completely lost. beta-Catenin but not N-cadherin was reinduced in brain endothelial cells during dedifferentiation in vitro and localized to the interendothelial junctions. These first in vivo data support the hypothesis that endothelial beta-catenin and N-cadherin are transiently relevant for the contact of brain endothelial to perivascular cells. Plakoglobin seems not to interact with N-cadherin but is exclusively localized at interendothelial junctions providing evidence for its role in the formation of stable adherens junctions, which may play a role for the initiation, and/or stabilization of tight junctions. Dev Dyn 2000;217:86-98.  (+info)

Labelling of retinal microglial cells following an intravenous injection of a fluorescent dye into rats of different ages. (6/301)

Retinal microglia were selectively and sequentially labelled in different layers of the retina of postnatal rats following a single intravenous injection of the fluorescent dye, rhodamine isothiocyanate (RhIc). The fluorescent cells were doubly immunostained with OX-42 and ED-1 antibodies that recognise complement type 3 (CR3) receptors and macrophage antigen, respectively. RhIc was first detected in the retinal blood vessels 5 min after injection. At 1 h, a variable number of microglia in the inner layers of the retina, namely, the nerve fibre and ganglion cell layers appeared to emit weak fluorescence. Labelled microglial cells in the inner nuclear and outer plexiform layers were not detected until 1 and 2 d had elapsed following RhIc injection. The number of labelled retinal microglia was progressively increased with time, peaking at 4 d after RhIc injection. The frequency of RhIc labelled cells also increased with age, with the largest number of cells occurring in 7-d-old rats but declined thereafter. In 11 d or older rats, RhIc was confined to the retinal blood vessels. It is concluded that when injected into the circulation, RhIc could readily gain access into the retina tissues due to an inefficient blood-retina barrier in early postnatal stages. It became impeded with maturation of the blood-retina barrier, which was established between 11 and 13 d of age. RhIc that inundated the retinal tissues was thoroughly sequestered by the resident microglial cells. It is therefore suggested that the latter could play a protective role against serum-derived substances that may be deleterious to the developing retina.  (+info)

Breakdown of the blood-retinal barrier induced by activated T cells of nonneural specificity. (7/301)

The cellular and microvascular responses of JC Lewis rats to an intravenous injection of activated T cells specific for ovalbumin were examined with the retinal whole mount technique. The retina was examined at various times post-injection (pi) with the use of antibodies to the alphabeta T cell receptor (TCR) or to major histocompatibility complex class II (MHC II), the monoclonal antibody ED1, and intravascular tracers. By 12 hours pi, small numbers of TCR(+), ED1(+), and MHC II(+) cells were present within the lumen of retinal vessels, and minor breakdown of the blood-retinal barrier (BRB) and microglial activation were evident. The intensity of these responses had increased by 1 day pi, when small numbers of TCR(+) cells had also undergone extravasation. By 2 to 3 days pi, the numbers of TCR(+), ED1(+), and MHC II(+) cells in the retinal parenchyma had increased, but the BRB breakdown and microglial activation had subsided. Thus, in the absence of target antigen, activated T cells induced limited and transient breakdown of the BRB, microglial activation, and the extravasation of ED1(+), MHC II(+) monocytes. In contrast, the retina of rats that received an intraocular injection of ovalbumin in addition to the intravascular injection of T cells showed massive cellular recruitment and breakdown of the BRB. These results indicate that an increase in the number of activated T cells in the circulation, such as that which occurs during viral or bacterial infection, has the potential to result in transient breakdown of the BRB and a mild local microglial response.  (+info)

Quantitative MR imaging study of intravitreal sustained release of VEGF in rabbits. (8/301)

PURPOSE: To determine whether sustained elevation of vascular endothelial growth factor (VEGF) in the vitreous cavity causes retinal hyperpermeability [blood-retinal barrier (BRB) breakdown] before the development of retinal neovascularization (NV) and to document the kinetics of the integrity of BRB breakdown versus time. METHODS: Poly(L-lactide-co-glycolide)based devices loaded with VEGF were implanted intravitreally in rabbit eyes. Contrast-enhanced magnetic resonance imaging (MRI) methods were used to identify and quantitate the retinal permeability at various time points after implantation. This was done with the newly developed MR tracer AngioMARK (Epix Medical, Boston, MA). After the MRI measurements, fundus photography and fluorescein angiography (FA) also were performed on the same set of animals. RESULTS: At 3 days after implantation, the MR images showed a significant retinal leakage into the vitreous cavity (BRB breakdown) of the VEGF-implanted eyes. To quantitate this leakage, the permeability surface area product (PS) was measured. At 3 days, the mean PS product was 1.25 +/-0.25 x 10(-5) cm3/min. Based on the VEGF in vitro release study, this 3-day BRB breakdown corresponded to a total sustained release of 7.42 +/- 0.54 microg/ml of VEGF. The fundus and FA photographs of these VEGF-implanted eyes taken at 4 days after implantation also showed a considerable level of retinal vascular dilation and tortuosity. By 12 days after implantation, the mean PS product decreased to 5.83 +/- 1.38 x 10(-6) cm3/min. However, the retinal NV was observed only after the second week after implantation. By this time, a total of 10.70 +/- 0.92 microg/ml of VEGF was released in a sustained fashion. Also, after the retinal NV development, retinal detachment also was observed. The control eyes, however, which were implanted with blank devices, remained unchanged and normal during the entire course of this study (PS = 5.57 +/- 0.66 x 10(-7) cm3/min). CONCLUSIONS. The findings indicate that sustained delivery of elevated amounts of VEGF in the vitreous cavity induces a BRB breakdown even earlier than 3 days after implantation. This was achieved after a total sustained release of 7.42 +/- 0.54 microg/ml of VEGF. This retinal leakage regressed by more than half by the time the retinal NV developed. Furthermore, a retinal detachment occurred after this retinal NV. These results are similar to proliferative diabetic retinopathy (PDR). The sustained elevation of VEGF in the vitreous cavity of rabbit eyes is potentially a good model to test VEGF antagonists to treat or prevent PDR in humans. The quantifiable change of BRB breakdown by the contrast-enhanced MRI method is ideal to assess the therapeutic intervention in vivo without killing the animal and may prove to be clinically useful in humans.  (+info)

The blood-retinal barrier, or the BRB, is part of the blood-ocular barrier that consists of cells that are joined tightly together to prevent certain substances from entering the tissue of the retina. It consists of non-fenestrated capillaries of the retinal circulation and tight-junctions between retinal epithelial cells preventing passage of large molecules from choriocapillaris into the retina. The blood retinal barrier has two components: the retinal vascular endothelium and the retinal pigment epithelium. Retinal blood vessels that are similar to cerebral blood vessels maintain the inner blood-ocular barrier. This physiological barrier comprises a single layer of non-fenestrated endothelial cells, which have tight junctions. These junctions are impervious to tracer, so many substances can affect the metabolism of the eyeball. The retinal pigment epithelium maintains the outer blood-retinal barrier. Diabetic retinopathy, eye damage that frequently occurs as a result of diabetes, is related ...
Purpose : In patients with ocular toxoplasmosis, disruption of retinal pigment epithelium is frequently observed. The retinal pigment epithelial layer constitutes outer blood retinal barrier (BRB) that lies between retina and leaky choroidal vasculature. In this study, we investigated the effect of monocytes infected with Toxoplasma gondii on in vitro model of outer BRB. Methods : Retinal pigment epithelial cells, ARPE-19, were cultivated on transwell to form a confluent monolayer. Then, human monocytic cells, THP-1, infected with Toxoplasma gondii or their conditioned medium were treated and the barrier function was evaluated by measurement of transepithelial electrical resistance (TEER) and immunocytochemistry of tight junction proteins. Additional treatment with FAK inhibitor (PF-573228) or neutralizing antibody against IL-8 was performed to investigate the associated signaling pathway. Results : Twenty-four hours after the treatment with infected monocytes or their conditioned medium, TEER ...
Breakdown of the blood-brain barrier (BBB) or inner blood-retinal barrier (BRB), induced by pathologically elevated levels of vascular endothelial growth factor (VEGF) or other mediators, can lead to vasogenic edema and significant clinical problems such as neuronal morbidity and mortality, or vision loss. Restoration of the barrier function with corticosteroids in the brain, or by blocking VEGF in the eye are currently the predominant treatment options for brain edema and diabetic macular edema, respectively. However, corticosteroids have side effects, and VEGF has important neuroprotective, vascular protective and wound healing functions, implying that long-term anti-VEGF therapy may also induce adverse effects. We postulate that targeting downstream effector proteins of VEGF and other mediators that are directly involved in the regulation of BBB and BRB integrity provide more attractive and safer treatment options for vasogenic cerebral edema and diabetic macular edema. The endothelial cell-specific
The purpose of this study was to characterize the cell surface proteome of native compared to cultured equine retinal pigment epithelium (RPE) cells. The RPE plays an essential role in visual function and represents the outer blood-retinal barrier. We are investigating immunopathomechanisms of equine recurrent uveitis, an autoimmune inflammatory disease in horses leading to breakdown of the outer blood-retinal barrier and influx of autoreactive T-cells into affected horses vitrei. Cell surface proteins of native and cultured RPE cells from eye-healthy horses were captured by biotinylation, analyzed by high resolution mass spectrometry coupled to liquid chromatography (LC MS/MS), and the most interesting candidates were validated by PCR, immunoblotting and immunocytochemistry. A total of 112 proteins were identified, of which 84% were cell surface membrane proteins. Twenty-three of these proteins were concurrently expressed by both cell states, 28 proteins exclusively by native RPE cells. Among the
The blood-retinal barrier (BRB) plays an important role in the homeostatic regulation of the microenvironment in the retina. It consists of inner and outer components, the inner BRB (iBRB) being formed by the tight junctions between neighbouring retinal capillary endothelial cells and the outer barrier (oBRB) by tight junctions between retinal pigment epithelial cells. Astrocytes, Müller cells and pericytes contribute to the proper functioning of the iBRB. In many clinically important conditions including diabetic retinopathy, ischaemic central retinal vein occlusion, and some respiratory diseases, retinal hypoxia results in a breakdown of the iBRB. Disruption of the iBRB associated with increased vascular permeability, results in vasogenic oedema and tissue damage, with consequent adverse effects upon vision. Factors such as enhanced production of vascular endothelial growth factor (VEGF), NO, oxidative stress and inflammation underlie the increased permeability of the iBRB and inhibition of ...
Purpose: VEGF-related signal transduction and gene regulatory networks play central roles in the vascular pathology of several retinal diseases: ROP, diabetic retinopathy, AMD, Norries disease and FEVR. While mechanisms are often explored in cell culture, there is need for in vivo models that are amenable to functional and molecular analysis during blood-retinal barrier (BRB) disruption and inflammatory response. We developed an intravitreal VEGF-injection model that provides a new platform for functional assessment of BRB disruption and countermeasures using ERG, Fluorescein angiography (FA) and Optical Coherence Tomography (OCT) in a single session of anesthesia.. Methods: Retinas of Long Evans rats were documented with bright-field imaging, FA, & OCT. Some animals received ERG, FA and OCT during a single session in an advanced ocular imaging suite of the Pediatric Retinal Research Laboratory. Subsequently, rats received a single intravitreal injection of recombinant human VEGF (35-gage ...
Rather than being a non-specific reaction to a noxious stimulus, breakdown of the capillary blood-retinal barrier causing macular edema appears to be dependent on a number of active processes which may be open to pharmacological manipulation. Extracellular influences which may affect barrier function include serum and neighboring cell types, which act though cytokines, such as vascular endothelial growth factor and transforming growth factor-ß, and other factors. A number of intracellular pathways acting on the cytoskeleton and components of the intercellular junctional complexes have been identified which mediate agonist-induced leak of the vascular endothelium. The further elucidation of these processes may be useful in the development of better treatments for breakdown of the inner blood-retinal barrier. ...
Researchers in Barcelona have developed a microfluidic chip that mimics the human blood-retinal barrier. The device contains several parallel compartments,
The device contains living cells and mimics the structure and physiological conditions of the blood-retinal barrier; it also enables testing...
Acute intensive insulin therapy is an independent risk factor for diabetic retinopathy. Here we demonstrate that acute intensive insulin therapy markedly increases VEGF mRNA and protein levels in the retinae of diabetic rats. Retinal nuclear extracts from insulin-treated rats contain higher hypoxia-inducible factor-1α (HIF-1α) levels and demonstrate increased HIF-1α-dependent binding to hypoxia-responsive elements in the VEGF promoter. Blood-retinal barrier breakdown is markedly increased with acute intensive insulin therapy but can be reversed by treating animals with a fusion protein containing a soluble form of the VEGF receptor Flt; a control fusion protein has no such protective effect. The insulin-induced retinal HIF-1α and VEGF increases and the related blood-retinal barrier breakdown are suppressed by inhibitors of p38 mitogen-activated protein kinase (MAPK) and phosphatidylinositol (PI) 3-kinase, but not inhibitors of p42/p44 MAPK or protein kinase C. Taken together, these findings ...
Acute intensive insulin therapy is an independent risk factor for diabetic retinopathy. Here we demonstrate that acute intensive insulin therapy markedly increases VEGF mRNA and protein levels in the retinae of diabetic rats. Retinal nuclear extracts from insulin-treated rats contain higher hypoxia-inducible factor-1α (HIF-1α) levels and demonstrate increased HIF-1α-dependent binding to hypoxia-responsive elements in the VEGF promoter. Blood-retinal barrier breakdown is markedly increased with acute intensive insulin therapy but can be reversed by treating animals with a fusion protein containing a soluble form of the VEGF receptor Flt; a control fusion protein has no such protective effect. The insulin-induced retinal HIF-1α and VEGF increases and the related blood-retinal barrier breakdown are suppressed by inhibitors of p38 mitogen-activated protein kinase (MAPK) and phosphatidylinositol (PI) 3-kinase, but not inhibitors of p42/p44 MAPK or protein kinase C. Taken together, these findings ...
Acute intensive insulin therapy is an independent risk factor for diabetic retinopathy. Here we demonstrate that acute intensive insulin therapy markedly increases VEGF mRNA and protein levels in the retinae of diabetic rats. Retinal nuclear extracts from insulin-treated rats contain higher hypoxia-inducible factor-1α (HIF-1α) levels and demonstrate increased HIF-1α-dependent binding to hypoxia-responsive elements in the VEGF promoter. Blood-retinal barrier breakdown is markedly increased with acute intensive insulin therapy but can be reversed by treating animals with a fusion protein containing a soluble form of the VEGF receptor Flt; a control fusion protein has no such protective effect. The insulin-induced retinal HIF-1α and VEGF increases and the related blood-retinal barrier breakdown are suppressed by inhibitors of p38 mitogen-activated protein kinase (MAPK) and phosphatidylinositol (PI) 3-kinase, but not inhibitors of p42/p44 MAPK or protein kinase C. Taken together, these findings ...
There are several mechanisms by which statins might exhibit anti-inflammatory effects in the eye [28]. Statins are known to inhibit the activation of Rho guanosine triphosphatase (GTPase), a key molecule in the endothelial ICAM-1-mediated pathway that facilitates lymphocyte migration [29-31]. Statins thus inhibit interactions between leukocytes and endothelial cells, preventing leukocyte transmigration from the vasculature, across the blood-retinal barrier [29, 32-34]. Endothelial cell nitric oxide synthase expression is up-regulated in the presence of statins, leading to higher levels of nitric oxide, which has protective effects on endothelial cells [35]. Statins also inhibit the formation of oxygen free radicals by endothelial cells [36, 37]. Thus, statins may act to stabilize the blood-ocular and blood-retinal barrier, transgression across which enables inflammatory mediators and immune activator cells to enter the anterior chamber, vitreous cavity, and retinal tissues. In addition, statins ...
The use of In vitro testing with living cells as an alternative to animal research has limitations like the difficulty to reproduce the interaction of cells. To
Placental Growth Factor Contributes to Micro-Vascular Abnormalization and Blood-Retinal Barrier Breakdown in Diabetic Retinopathy. Kowalczuk, Laura; Touchard, Elodie; Omri, Samy; Jonet, Laurent; Klein, Christophe; Valamanes, Fatemeh; Berdugo, Marianne; Bigey, Pascal; Massin, Pascale; Jeanny, Jean-Claude; Behar-Cohen, Francine // PLoS ONE;2011, Vol. 6 Issue 3, p1 Objective: There are controversies regarding the pro-angiogenic activity of placental growth factor (PGF) in diabetic retinopathy (DR). For a better understanding of its role on the retina, we have evaluated the effect of a sustained PGF overexpression in rat ocular media, using ciliary muscle... ...
Discussion. The present study demonstrated the functional involvement of SR-BI in the uptake of HDL-associated α-tocopherol by retinal capillary endothelial cells using an in vitro inner BRB model, TR-iBRB2 cells. Although the uptake process of fat-soluble micronutrients like vitamin E was assumed to be passive diffusion across the plasma membrane, recent reports have proposed SR-BI-mediated transport of α-tocopherol in the brain capillary endothelial cells and enterocytes [18,19,21]. In this study, [14C]α-tocopherol-HDL uptake by TR-iBRB2 cells exhibited a time-dependent increase and did not reach "steady-state" at least for 90 min, suggesting that, for the most part [14C]α-tocopherol-HDL uptake by TR-iBRB2 cells depends on influx mechanism(s). [14C]α-tocopherol-HDL uptake by TR-iBRB2 cells was reduced by 88% for 90 min at 4 °C compared with that at 37 °C (Figure 1A). This suggests the involvement of an energy-dependent carrier-mediated process, rather than passive diffusion. In turn, ...
Advanced glycation end products have been associated with numerous complications of diabetes (Ahmed, 2005). The levels of AGEs in the blood and vitreous humor of diabetic patients have been correlated with the clinical progression of diabetic retinopathy (Yokoi et al., 2005). Although the RPE expresses several pattern-recognizing receptors activated by AGEs, a direct causal relationship between AGEs and RPE dysfunction has not been addressed before. Using human glycated-albumin, we determined the effect of AGEs on the barrier function of the RPE. The RPE constitutes the outer blood-retina barrier and is responsible for fluid transport from the neural retina to the choroid. This transport counters the Starling forces across the RPE that drive fluid toward the retina (Maepea, 1992). As a result, increasing RPE permeability can contribute to the development of macular edema, a key component of diabetic retinopathy.. Our experiments demonstrated that the administration of human Glyc-alb reduced TEER ...
• The permeability of the blood-retina barrier was tested in rats with early streptozocin-induced diabetes. Two different tracer substances were used: fluoresce
Chronic hyperglycemia may cause growth factor alterations that are likely to participate in tissue remodeling typical for diabetic late complications. However, few details of such events are known. The ocular vitreous fluid allows studies of growth factor levels in human eyes (after vitrectomy). The vitreous is highly inert and protected by the blood-retina barrier and thus probably reflects growth factor production by the normal retina. Vitreous from patients with proliferative diabetic retinopathy (PDR) was compared with vitreous obtained from patients with nonproliferative eye disease and with vitreous from patients without diabetes but with marked neovascular proliferations due to ischemia. This design permits us to distinguish diabetes-related from non-diabetes-related alterations. Insulin-like growth factor I (IGF-I), IGF-II, IGF binding protein 2 (IGFBP-2), and IGFBP-3 were elevated 3-to 13-fold in nondiabetic retinal ischemia and 1.5- to 3-fold in PDR, indicating that the changes were ...
Névroglie 0 questions The non-neuronal cells of the nervous system. They not only provide physical support, but also respond to injury, regulate the ionic and chemical composition of the extracellular milieu, participate in the BLOOD-BRAIN BARRIER and BLOOD-RETINAL BARRIER, form the myelin insulation of nervous pathways, guide neuronal migration during development, and exchange metabolites with neurons. Neuroglia have high-affinity transmitter uptake systems, voltage-dependent and transmitter-gated ion channels, and can release transmitters, but their role in signaling (as in many other functions) is unclear. ...
|p|Many antioxidants, even some of the more potent ones, are unable to cross both your blood-brain and blood-retinal barriers to reach your brain, nervous system, and eyes.|/p| |p|Astaxanthin is different. It has the rare ability to cross these protectiv
The monolayer of endothelial cells lining the vessel wall forms a semipermeable barrier (in all tissue except the relatively impermeable blood-brain and inner retinal barriers) that regulates tissue-fluid homeostasis, transport of nutrients, and migration of blood cells across the barrier. Permeabil …
In choosing a model for evaluating the data for the present study, we faced a dilemma between an unbiased representation of the data and a parsimonious description of the essential physiological phenomena. The model used in the present study is based on simplifying assumptions. For example, the transit time of the nonexchanging ("large") vessels, t0, is assumed to be uniform and identical for sodium and rubidium. The membrane permeability for rubidium and the diameter of sinusoids are also assumed uniform. These simplifications may be responsible for small but systematic deviations of the model from the experimental data. Moreover, temporal fluctuations of liver blood flow due to the breathing movements of the animals may have led to minor distortions of the outflow profiles. Since for a majority of the animals, systematic deviations were not significant, the values obtained for the permeability surface area product may be regarded as valid approximations for the liver averages in all ...
The retinal pigment epithelium (RPE), the outer blood-retinal barrier in the eye, secretes many growth factors to support the normal functions of both the retina and the choroid. Dysfunction of RPE is believed to play a critical role in the pathogenesis of age-related macular degeneration (AMD). Advanced AMD can manifest in either geographic atrophy (dry AMD) or a neovascular form of the disease (wet AMD). Recently our studies indicated that bone morphogenetic protein-4 (BMP4), one growth factor of the transforming growth factor-β (TGF-β) superfamily, may be involved in the molecular switch that determines which advanced form of AMD an individual develops. We demonstrated that BMP4 was highly expressed in the macular RPE and adjacent extracellular matrix of dry AMD patients, and BMP4 mediated oxidative stress induced RPE cell senescence in vitro. However, BMP4 was immunohistochemically absent in RPE in subretinal choroidal neovascularization (CNV) membranes of wet AMD patients. This work ...
Objective and design A mathematical analysis of leukocytes accumulating in experimental autoimmune uveitis (EAU), using ordinary differential equations (ODEs) and incorporating a barrier to cell traffic. Materials and subjects Data from an analysis of the kinetics of cell accumulation within the eye during EAU. Methods We applied a well-established mathematical approach that uses ODEs to describe the behaviour of cells on both sides of the blood-retinal barrier and compared data from the mathematical model with experimental data from animals with EAU. Results The presence of the barrier is critical to the ability of the model to qualitatively reproduce the experimental data. However, barrier breakdown is not sufficient to produce a surge of cells into the eye, which depends also on asymmetry in the rates at which cells can penetrate the barrier. Antigen-presenting cell (APC) generation also plays a critical role and we can derive from the model the ratio for APC production under inflammatory ...
FT011M reduced retinal leukostasis and ICAM-1 mRNA levels in Ren-2 rats diabetic for 8 weeks.Non-diab, non-diabetic. Diab, diabetic. V, vehicle. (A to C) Microg
OBJECTIVE: To assess the effects of bevacizumab and everolimus, individually and combined, on CT perfusion (CTp) parameters in liver metastases from neuroendocrine tumors (mNET) and normal liver. METHODS: This retrospective study comprised 27 evaluable patients with mNETs who had participated in a two-arm randomized clinical trial of mono-therapy with bevacizumab (Arm B) or everolimus (Arm E) for 3 weeks, followed by combination of both targeted agents. CTp was undertaken at baseline, 3 and 9 weeks, to evaluate blood flow (BF), blood volume (BV), mean transit time (MTT), permeability surface area product (PS), and hepatic arterial fraction (HAF) of mNET and normal liver, using a dual-input distributed parameter physiological model ...
The RPE stores vitamin A, a precursor of the photopigments, and thus participates in their regeneration. There are four photopigments which are all bleached on exposure to light: rhodopsin (found in the rods, for night vision) and one for each of the three different types of cones (one for each of the primary colours). It synthesises glycosaminoglycans for the interphotoreceptor matrix, i.e. the material lying between and separating the photoreceptors.. Besides oxygen, the RPE selectively transports nutrients from the choroid to supply the outer third of the retina and removes the waste products of photoreceptor metabolism to be cleared by the choroidal circulation. By selective pumping of metabolites and the presence of its tight intercellular junctions, the RPE acts as a barrier, called the blood-retinal barrier, preventing access of larger or harmful chemicals to retinal tissue, thereby contributing to the maintenance of a stable and optimal retinal environment.8,9,10. The RPE has complex ...
The RPE stores vitamin A, a precursor of the photopigments, and thus participates in their regeneration. There are four photopigments which are all bleached on exposure to light: rhodopsin (found in the rods, for night vision) and one for each of the three different types of cones (one for each of the primary colours). It synthesises glycosaminoglycans for the interphotoreceptor matrix, i.e. the material lying between and separating the photoreceptors.. Besides oxygen, the RPE selectively transports nutrients from the choroid to supply the outer third of the retina and removes the waste products of photoreceptor metabolism to be cleared by the choroidal circulation. By selective pumping of metabolites and the presence of its tight intercellular junctions, the RPE acts as a barrier, called the blood-retinal barrier, preventing access of larger or harmful chemicals to retinal tissue, thereby contributing to the maintenance of a stable and optimal retinal environment.8,9,10. The RPE has complex ...
We report the second family recognised to have autosomal dominant vitreoretinochoroidopathy. The clinical features were (1) autosomal dominant inheritance; (2) peripheral, coarse pigmentary degeneration of the fundus for 360 degrees, with a relatively discrete posterior border in the equatorial region (this finding may be pathognomonic); (3) superficial punctate yellowish-white opacities in the retina; (4) various vascular abnormalities; (5) breakdown of the blood-retinal barrier; (6) retinal neovascularisation; (7) vitreous abnormalities; and (8) choroidal atrophy. Visual reduction was mainly due to macular oedema or vitreous haemorrhage. ...
One of the really special attributes of astaxanthin is its ability to cross the blood-brain and blood-retinal barrier to protect both the brain and eyes. This effect is quite unusual for carotenes. For example, popular carotenes like beta-carotene and lycopene do not cross either barrier. This effect of astaxanthin indicates that it may be particularly helpful in improving brain and eye health as well as protecting the brain against Alzheimers disease, macular degeneration, and other degenerative brain and eye disorders. Of course, it has other benefits as well, but my feelings are that this ability to cross into the brain and retina is what makes it really special.. Another interesting effect of astaxanthin is on red blood cells. Because red blood cells (RBCs) are more susceptible to being damaged by oxidative attack as we age, this can lead to impaired delivery of oxygen to our tissues. Astaxanthins effects on cell membranes may be especially important in RBCs. In a 2011 double-blind ...
Purpose: The outer limiting membrane (OLM) is considered to play a role in maintaining the structure of the retina through mechanical strength. However, the observation of junction proteins located at the OLM and its barrier permeability properties may suggest that the OLM may be part of the retinal barrier. Material and methods: Normal and diabetic rat, monkey, and human retinas were used to analyze junction proteins at the OLM. Proteome analyses were performed using immunohistochemistry on sections and flat-mounted retinas and western blotting on protein extracts obtained from laser microdissection of the photoreceptor layers. Semi-thin and ultrastructure analyses were also reported. Results: In the rat retina, in the subapical region zonula occludens-1 (ZO-1), junction adhesion molecule (JAM), an atypical protein kinase C, is present and the OLM shows dense labeling of occludin, JAM, and ZO-1. The presence of occludin has been confirmed using western blot analysis of the microdissected OLM region. In
Everything youll probably ever need to know about safer sex barriers, like which to use, how to use them, how to get more comfortable with them, and how surprisingly cute they are.
Everything youll probably ever need to know about safer sex barriers, like which to use, how to use them, how to get more comfortable with them, and how surprisingly cute they are.
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
Approach and Results-Pregnant Sprague Dawley rats were fed LS (0.03% NaCl) or normal salt (0.3% NaCl) diets, and ischemic retinopathy was induced in the offspring. An LS diet reduced retinal neovascularization and vaso-obliteration, the mRNA and protein levels of the angiogenic factors, vascular endothelial growth factor, and erythropoietin. Microglia, which influence vascular remodeling in ischemic retinopathy, were reduced by LS as was tumor necrosis factor-α. Macroglial Müller cells maintain the integrity of the blood-retinal barrier, and in ischemic retinopathy, LS reduced their gliosis and also vascular leakage. In retina, LS reduced mineralocorticoid receptor, angiotensin type 1 receptor, and renin mRNA levels, whereas, as expected, plasma levels of aldosterone and renin were increased. The aldosterone/mineralocorticoid receptor-sensitive epithelial sodium channel alpha (ENaCα), which is expressed in Müller cells, was increased in ischemic retinopathy and reduced by LS. In cultured ...
article{1898628, abstract = {Objective: Computed tomography (CT) perfusion studies can provide valuable information regarding tumor vascularization. We report on a study assessing CT perfusion characteristics in the normal pancreas and in patients with pancreatic adenocarcinoma. Methods: Twenty healthy subjects and 20 patients with histologically confirmed pancreatic adenocarcinoma were included in the study after written informed consent and approval by our institutional review board. All subjects underwent perfusion CT imaging of the pancreas using 128-slice dual-source CT. The scanning sequence included 18 scans. Parametric maps of blood volume (BV), blood flow (BF), and permeability surface area product (PS) were generated and compared with density measurements. Results: In normal pancreas, no significant difference in perfusion values was observed between head, body, and tail of the pancreas. Mean organ values were 76.76 (SD, 15.6) mL/100 g/min, 15.80 (SD, 2.40) mL/100 g, and 27.74 (SD, ...
Symptoms of Retinal edema including 2 medical symptoms and signs of Retinal edema, alternative diagnoses, misdiagnosis, and correct diagnosis for Retinal edema signs or Retinal edema symptoms.
Macular oedema is an accumulation of fluid within the central part of the retina (the macula). This can lead to loss of the normal architecture and function of the macula causing distortion and deterioration of central vision. Macular oedema results from a breakdown in the blood-retinal barrier, with fluid accumulating both interstitially and within the retinal glial cells (Müller cells). It can occur in patients with diabetic retinopathy, retinal vein occlusions or ocular inflammation (uveitis). Macular oedema is diagnosed clinically and monitored with optical coherence tomography (Box 1, Figure 1 and Figure 2).. ...
Oxidative Medicine and Cellular Longevity is a unique peer-reviewed, Open Access journal that publishes original research and review articles dealing with the cellular and molecular mechanisms of oxidative stress in the nervous system and related organ systems in relation to aging, immune function, vascular biology, metabolism, cellular survival and cellular longevity. Oxidative stress impacts almost all acute and chronic progressive disorders and on a cellular basis is intimately linked to aging, cardiovascular disease, cancer, immune function, metabolism and neurodegeneration. The journal fills a significant void in todays scientific literature and serves as an international forum for the scientific community worldwide to translate pioneering
Acute stroke has a major effect on the cerebral vasculature with disruption of the neurovascular unit, leading to vasogenic edema. Breakdown of the blood-brain barrier (BBB) in ischemic stroke occurs in the early phases of ischemia, and is accentuated by IV treatment with recombinant tissue plasminogen activator, which increases the risk of hemorrhagic transformation and intracerebral hemorrhage.1,2 In a serendipitous observation using fluid-attenuated inversion recovery (FLAIR) MRI, gadolinium-DTPA enhancement of the CSF space overlying the ischemic tissue indicated greater stroke severity, increased age of the patient, and reperfusion injury. They called this phenomenon hyperintense acute reperfusion marker (HARM), and now Hitomi et al.3 have extended the original study to show enhancement of the structures in the eye. In addition to the endothelial blood-CNS barriers that maintain CNS homeostasis, regulate nutrition and detoxification, as well as immune cell trafficking into the brain and ...
Figure 1. Differential display analysis of TR-iBRB and TR-BBB cells. A: Typical fluorescent image of polyacrylamide gel electrophoresis. An arrow indicates selectively expressed DNA bands in TR-iBRB cells. DNA bands were cloned and sequenced. B: Nucleotide sequence of the selectively expressed clone (clone 1) marked by the arrow in A. Clone 1 sequence after nucleotide position 72 has 77% nucleotide homology with the 3 terminal of the mouse M-cadherin gene.. ...
Assessment of Blood-Brain Barrier Breakdown. Animal Models of Acute Neurological Injuries II: Injury and Mechanistic Assessments, Volume 1. 401-413. 2012 ...
Diabetes mellitus is associated with an increase in proliferative lesions in the small cerebral vessels.1 Functionally, the blood-retinal barrier is closely related to the blood-brain barrier (BBB)2 and cortical capillaries in experimental models of diabetes exhibit similar microangiopathy to that found in the human retina in diabetes.3, 4. A principal neuroradiological feature that may be associated with cerebral microvascular disease is "white matter hyperintensities" or "leukoaraiosis", a mixed condition of uncertain aetiology manifested on CT scans as hypodensity in the cerebral white matter, and as hyperintensities on T2, proton density or fluid attenuated inversion recovery (FLAIR) MR imaging.5 Recent longitudinal studies have highlighted diabetes as a risk factor for dementia, doubling the risk of senile dementia of the Alzheimer type.6 Several studies have established a correlation between the presence and extent of white matter hyperintensities and cognitive impairment, ranging from ...
Rat Retinal Microvascular Endothelial Cells from Creative Bioarray are isolated from retinal tissue of 6-8 week old laboratory Sprague-Dawley rat. Rat Retinal Microvascular Endothelial Cells are grown in T75 tissue culture flasks pre-coated with gelatin-based coating solution for 2 min and incubated in Creative Bioarray Culture Complete Growth Medium generally for 3-7 days. Cultures are then expanded. Prior to shipping, cells at passage 3 are detached from flasks and immediately cryo-preserved in vials. Each vial contains at least 1x10^6 cells per ml and is delivered frozen. The method we use to isolate endothelial cells was developed based on a combination of established and our proprietary methods. These cells are pre-coated with PECAM-1 (CD31) antibody, following the application of magnetic beads pre-coated with secondary antibody ...
Principal Investigator:Takagi Hitoshi, Project Period (FY):2014-04-01 - 2017-03-31, Research Category:Grant-in-Aid for Scientific Research (C), Section:一般, Research Field:Ophthalmology
Hyperglycemia-induced inflammation causes the dysfunction of blood vessels, and Toll-like receptor 4 (TLR4) plays a key role in inflammation-induced angiogenesis. However, the impact of TLR4 on the pathogenesis of diabetic retinopathy (DR) is poorly understood. In this study, we examined the expression of TLR4 in retinal vascular endothelial cells of patients with DR and diabetic mice, and explored the role of TLR4 in mediating inflammatory responses by human microvascular endothelial cells (HMEC-1) under high-glucose condition. The expression of TLR4 in retinal vascular endothelial cells of patients with proliferative diabetic retinopathy and diabetic mice induced by streptozotocin was examined using immunofluorescence. HMEC-1 cells were cultured and the expression of TLR4, MyD88 and Interleukin-1β (IL-1β) was examined under high-glucose condition. Endothelial cells with TLR4 silencing and antagonist of TLR4 as well as endothelial cells from TLR4 deficient mice were used to study the effect of
Quantification of Zonula Occludens-1 mRNA expression in cultu-red bovine retinal endothelial cells, using SYBR green real-time PCR, Sekaran Muniandy, Koon Chu Yaiw, Jack Bee Chook,
TY - JOUR. T1 - Clinical Characteristics and Prognostic Factors in Ankylosing Spondylitis Associated Uveitis. AU - Lee, Ji Hwan. AU - Choi, Moonjung. AU - Rim, Tyler Hyung Taek. AU - Lee, Sung Chul. AU - Lee, Christopher Seungkyu. PY - 2019/1/2. Y1 - 2019/1/2. N2 - Purpose: To identify the clinical features and prognostic factors of uveitis associated with ankylosing spondylitis (AS). Methods: This retrospective, interventional case series study reviewed the medical records of 91 AS patients with uveitis. Results: The characteristics of AS-associated uveitis included male preponderance (70%), average onset in the fourth decade, unilateral manifestation (87.9%), and vitreous involvement or retinal vascular leakage (36.3%). All patients had acute anterior uveitis. The best corrected visual acuity in logMAR improved from 0.8 ± 0.3 to 0.1 ± 0.2. The use of biologic agents was the only significant factor in the multivariate analysis. Patients with vitreous involvement/retinal vascular leakage were ...
Diabetic retinopathy is one of the leading causes of vision loss in industrialized countries. Despite recent advances, the biochemical basis for the development of this diabetic complication is uncertain. Although retinal circulation is unique in that it is readily observable noninvasively, retinal tissue is extremely difficult to study in humans because of the problems inherent in obtaining fresh, appropriate biopsy material. Moreover, because of the difficulties in working with animal models of diabetic retinopathy, such as the dog, many investigators have turned to cell-culture models, especially those using primary cultures of retinal capillary endothelial cells and pericytes. Diabetic retinopathy involves both morphological and functional changes in the retinal capillaries. Morphological changes include basement membrane thickening and pericyte disappearance; functional changes include one important early change-increased permeability-which may be attributable to endothelial cell changes ...
Eye drops are the most acceptable dosage form by ocular route, which as has disadvantage of bioavailability. The anatomical and physiological constrains limited permeability of drug such as drug loss from the ocular surface by lachrymal drainage, blood-ocular barriers. A number of drug delivery system has been developed to improve the bioavailability and to prolong the residence time of drugs on the eye. Such as promising system for ocular drug delivery is a microemulsion. Microemulsions are clear, stable, isotropic mixtures of oil, water and surfactant, frequently in combination with a cosurfactant. This review gives an overview of the potential of microemulsions as delivery vehicles for eye. Both lipophilic and hydrophilic characteristics are present in microemulsions, so that the loaded drugs can diffuse passively as well get significantly partitioned in the variable lipophilic-hydrophilic corneal barrier.
5. The BRB throughout these proceedings has relied on section 727.203(b)(2), which allows rebuttal by a showing that "the individual is able to do his usual coal mine work or comparable and gainful work." In previously reversing the ALJ, the BRB stated that under section 727.203(b)(2), "a party can rebut the presumption through evidence proving that the only impairment that can cause compensable disability (i.e., a respiratory or pulmonary impairment) is either non-existent or not totally disabling." Kertesz I, 3 B.L.R. at 1-369 to 1-370. In reversing the decision we review here, the BRB has again applied section 727.203(b)(2). Kertesz II, 8 B.L.R. at 1-115 & n. 3. Because it is undisputed that Kertesz is totally disabled and unable to do his usual coal mine work or comparable and gainful work, we believe the BRB erred in invoking section 727.203(b)(2). We believe, to the contrary, that evidence showing the presumed disease does not exist goes to rebuttal under section 727.203(b)(4) ("evidence ...
The proposed study will be performed in patients with a proven lung cancer for whom induction therapy and subsequent surgical resection of any kind is planned. Kinetic analysis of dynamic contrast-enhanced CT will performed using the CT Perfusion 3 software (General Electric Medical Systems), yielding parameters characterizing tumor microvasculature in terms of the vascularity, or the blood volume (BV), the tumor perfusion or blood flow (BF), and the immaturity of the vascular wall, in terms of the microvascular permeability (permeability surface area, PS).. To test the assumption that dynamic CT-assessed tumor microvascular characteristics represent reliable, user-independent and reproducible parameters, microvascular values and parameter maps will be derived from two independent observers. To address the interobserver variability, each study will be analyzed by the PI and by a second researcher (blinded to the results of the PI). Kappa-statistics will be used to assess inter-rater ...
Ocular diseases characterized by retinal neovascularization are among the principal causes of visual loss worldwide. In an effort to understand the components of the retinal angiogenesis and its regulation by various molecules, I developed a procedure to isolate retinal microvascular endothelial cells (EC) and pericytes from ...
Affiliation:関西医科大学,医学部,講師, Research Field:Ophthalmology,Ophthalmology, Keywords:VEGF,PEDF,糖尿病網膜症,血管新生,diabetic retinopathy,angiogenesis,細胞接着分子,脈絡膜新生血管,leukostasis,加齢, # of Research Projects:6, # of Research Products:35
19:57, 19 November 2007 [email protected] (talk , contribs , logs) edited Thames Barrier ( Description Removed ref that says nothing about how many times the barrier has been closed; doesnt even mention barrier) ...
Two cases of retinal detachment in commotio retinae are presented. Both had a successful outcome with scleral buckling alone, without subretinal fluid drainage or retinopexy.. A 22-year-old man was referred to our unit 2 days after blunt trauma to his right eye. On examination, his visual acuities were 6/9 and 6/6 in the right and left eyes, respectively. Abnormal findings included mild right traumatic uveitis, a mild right vitreous haemorrhage, and a large area of superotemporal commotio retinae in the detached retina, and no posterior vitreous detachment. This was associated with a large peripheral retinal tear, extending from 10:00 to 12:00 h. As signs of progression were noted while the macula remained attached, the patient underwent scleral buckling surgery with a type 277 scleral buckle. To prevent further inflammation and breakdown of the blood-retinal barrier, neither cryotherapy nor subretinal fluid ...
Elevated inflammatory cytokines contribute to the pathogenesis of various retinal diseases such as diabetic retinopathy, retinal vasculitis and retinitis. However, the underlying mechanism of retinal inflammation remains largely unknown. Recent studies demonstrated that acetylcholinesterase (ACHE) is an inflammatory indicator in central neural system. This study was aimed to dissect the role of ACHE in retinal inflammation, and its mechanism of action. Retinal inflammation was induced by intravitreal injection of tumor necrosis factor-α (TNF-α) in heterozygous ACHE knockout mice (ACHE+/-) and wild type mice (ACHE+/+). Donepezil, a well-known ACHE inhibitor, was administrated by daily gavage. Expression of ACHE and intercellular adherent molecule-1 (ICAM-1), infiltration of CD11b+ inflammatory cells, retinal leukostasis and vascular leakage was determined in both ACHE ± and ACHE+/+ mice. ARPE-19â ¯cells, a human retinal pigment epithelial cell line, were cultured for in vitro assay. ...
Trypsin digest is one of the most commonly used methods to analyze retinal vasculature. This manuscript describes the method in detail, ...
Screen for life can check for early diabetes, high cholesterol, hypertension, colon and cervical cancer at affordable rates. At Punggol, Singapore 2017
Apparatus and process for separating a fluid mixture into less permeable and more permeable fractions employing novel selectively permeable barriers comprised of a porous, emulsion treated substrate and a non-porous selectively permeable barrier layer thereon.
Kielczewski, J., Calzi, S., Shaw, L., Cai, J., Qi, X., Ruan, Q., Wu, L., Liu, L., Hu, P., Chan-Ling, T., Firth, S., Baxter, R., et al (2011). Free insulin-like growth factor binding protein-3 (IGFBP-3) reduces retinal vascular permeability in association with a reduction of acid sphingomyelinase (ASMase). Investigative Ophthalmology and Visual Science, 52(11), 8278-8286. [More Information] ...
TY - JOUR. T1 - BIGH3 protein and macrophages in retinal endothelial cell apoptosis. AU - Mondragon, Albert A.. AU - Betts-Obregon, Brandi S.. AU - Moritz, Robert J.. AU - Parvathaneni, Kalpana. AU - Navarro, Mary M.. AU - Kim, Hong Seok. AU - Lee, Chi Fung. AU - Lebaron, Richard G.. AU - Asmis, Reto. AU - Tsin, Andrew T.. PY - 2015/1. Y1 - 2015/1. N2 - Diabetes is a pandemic disease with a higher occurrence in minority populations. The molecular mechanism to initiate diabetes-associated retinal angiogenesis remains largely unknown. We propose an inflammatory pathway of diabetic retinopathy in which macrophages in the diabetic eye provide TGFβ to retinal endothelial cells (REC) in the retinal microvasculature. In response to TGFβ, REC synthesize and secrete a pro-apoptotic BIGH3 (TGFβ-Induced Gene Human Clone 3) protein, which acts in an autocrine loop to induce REC apoptosis. Rhesus monkey retinal endothelial cells (RhREC) were treated with dMCM (cell media of macrophages treated with high ...
PURPOSE: Advanced glycation endproduct (AGE) formation on the basement membrane of retinal capillaries has been previously described but the impact of these adducts on capillary endothelial cell function vascular repair remains uncertain. This invest
Olmesartan reduced the risk of microalbuminuria by 23% in normoalbuminuric patients with Type 2 diabetes and at least one additional cardiovascular
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Rizzolo, LJ (1997). "Polarity and the development of the outer blood-retinal barrier.". 》Histology and Histopathology》 12 (4): ... 망막색소상피세포는 혈액 망막 장벽 (Blood Retina Barrier, BRB)를 형성한다. 망막색소상피세포는 세포 간에 밀착연접 (tight junction)으로 연결된 상태이며, 이러한 결합을 통하여 다른 신체 조직들에 ... Rizzolo, lj (2014). "Barrier properties of cultured retinal pigment epithelium". 》Experimental Eye Research》 126: 16-26. PMID ... 망막색소상피세포(Retinal Pigment Epithelium cells, RPE cells)는 망막 감각신경 부분의 바깥에 존재하며, 색소가 있는 세포들을 지칭한다. [1] ...
2001). "VEGF-initiated blood-retinal barrier breakdown in early diabetes". Invest Ophthalmol Vis Sci. 42: 2408-2413. Vascular ... VEGF's normal function is to create new blood vessels during embryonic development, new blood vessels after injury, muscle ... VEGFxxx may then cause the creation of new blood vessels in the retina and elsewhere in the eye, heralding changes that may ... Solid cancers cannot grow beyond a limited size without an adequate blood supply; cancers that can express VEGF are able to ...
"The Retinal Pigment Epithelium: Something More than a Constituent of the Blood-Retinal Barrier?Implications for the ... Closely applied to retinal internal limiting membrane. Firm attachment sites: Along blood vessels and at sites of retinal ... Therefore, if blood, cells or other byproducts of inflammation get into the vitreous, they will remain there unless removed ... The vitreous humour contains no blood vessels, and 98-99% of its volume is water (as opposed to only 75% in the cornea). In ...
12th International Symposium Signaling at Blood Brain and Blood Retinal Barrier, Invited lecturer, United Kingdom (2009) The ... "AKAP12 regulates human blood-retinal barrier formation by downregulation of HIF-1a". Journal of Neuroscience. 27: 4472-4481. ... "SSeCKS regulates angiogenesis and tight junction formation in blood-brain barrier". Nature Medicine. 9: 900-906. doi:10.1038/ ... Seoul Brain Barrier Symposium, Organizer, South Korea (2012) Myoung Sook Kim; Ho Jeong Kwon; You Mie Lee; Jin Hyen Baek; Jae- ...
Chang YH, Chen PL, Tai MC, Chen CH, Lu DW, Chen JT (Aug 2006). "Hyperbaric oxygen therapy ameliorates the blood-retinal barrier ... HBO treatment of individuals who have cancer presents a problem, since HBO both increases blood flow via angiogenesis and also ... Because the hemoglobin of the red blood cells is almost saturated with oxygen at atmospheric pressure, this route of transport ... At normal atmospheric pressure, oxygen transport is limited by the oxygen binding capacity of hemoglobin in red blood cells and ...
... clinical relevance and in vitro analysis of the function of the outer blood-retinal barrier". Developments in Ophthalmology. ... Under the trade name Brilliant Peel, Brilliant Blue G is used as a stain to assist surgeons in retinal surgery.[27] ...
"Matrix metalloproteinases in early diabetic retinopathy and their role in alteration of the blood-retinal barrier". Laboratory ... The increase in blood-brain barrier and blood-spinal cord barrier permeability allows for more neutrophils to infiltrate the ... MMP-3 also does damage to the blood-spinal cord barrier (BSCB), the functional equivalent of the blood-brain barrier, after ... Lee JY, Choi HY, Ahn HJ, Ju BG, Yune TY (Nov 2014). "Matrix metalloproteinase-3 promotes early blood-spinal cord barrier ...
"The Retinal Pigment Epithelium: Something More than a Constituent of the Blood-Retinal Barrier? Implications for the ...
"Neuroprotective and Blood-Retinal Barrier-Preserving Effects of Cannabidiol in Experimental Diabetes". The American Journal of ... doi:10.1182/blood-2004-03-1182. PMID 15454482. *↑ Casanova ML; Blázquez C; Martínez-Palacio J; Villanueva, Concepción; ...
Something More than a Constituent of the Blood-Retinal Barrier-Implications for the Pathogenesis of Diabetic Retinopathy". ... They are the only retinal glial cell that shares a common cell lineage with retinal neurons. However, a subset of Müller glia ... Damage to retinal cells results in Müller cells to undergo gliosis. The result of the response varies depending on the damage ... They are to be critical to the development of the retina in mice, serving as promoters of retinal growth and histogenesis via a ...
... retinal ganglion cells MeSH A09.371.729.775 --- retinal horizontal cells MeSH A09.371.894.030 --- blood-aqueous barrier MeSH ... blood-retinal barrier MeSH A09.371.729.313 --- fundus oculi MeSH A09.371.729.522 --- macula lutea MeSH A09.371.729.522.436 --- ...
... the brain sits behind the blood-brain barrier and the retina sits behind the blood-retinal barrier) and so do not normally have ... PIOL affects the sub-retinal pigment epithelium (RPE), can invade into the retina, the vitreous, and the optic nerve. ...
By analogy to Coats disease, the exudative retinopathy is thought to result from breakdown of the blood-retinal barrier at the ... If not treated, the retinal detachment can lead to ischemia and growth of new blood vessels over the iris and anterior chamber ... Laser coagulation or cryoablation (freezing) of the retina can be used to destroy the abnormal blood vessels. Retinal ... Characteristically, the abnormal vessels are localized and the retinal blood vessels peripheral to the abnormal ones seemingly ...
... including those that cannot cross the blood-brain barrier or the blood-retinal barrier on their own. Within this approach, ... "Comparative physiology of the blood-brain barrier". In Suckling, A.J.; Rumsby, M.G.; Bradbury, M.W.B. The Blood-Brain Barrier ... "Quantitation of blood-brain barrier permeability". In Neuwelt, E.A. Implications of the Blood-Brain Barrier and its ... Blood-Brain Barrier in Psychology and Medicine. Raven Press, New York. Bradbury, M. (1979). The Concept of a Blood-Brain ...
... model of human ROP has shown that beta-blockade is protective against retinal angiogenesis and ameliorate blood-retinal barrier ... It is thought to be caused by disorganized growth of retinal blood vessels which may result in scarring and retinal detachment ... The stage of ROP refers to the character of the leading edge of growing retinal blood vessels (at the vascular-avascular border ... Examination of the retina of a premature infant is performed to determine how far the retinal blood vessels have grown (the ...
Epithelial transport: As mentioned above, RPE compose the blood-retinal barrier, the epithelia has tight junctions between the ... First, it represents a mechanical and tight barrier which separates the inner space of the eye from the blood stream. Second, ... This comes not directly from the visual cycle but from several retinal pools of retinal binding proteins which are connected to ... This is important for the immune privilege (not only as barrier, but with signalling process as well) of eyes, a highly ...
Blood-air barrier Blood-brain barrier Blood-ocular barrier Blood-retinal barrier Blood-testis barrier Blood-thymus barrier ...
... and stabilization of the blood retinal barrier were reported anecdotally in the management of macular telangiectasia type 1. In ... refractile deposits in the superficial retinal layers-may be seen within the affected area.a focal area of diminished retinal ... it has been speculated that chronic venous congestion caused by obstruction of the retinal veins as they cross retinal arteries ... either due to intra-retinal edema and serous retinal detachment (Type 1) or pigmented RPE scar formation or neovascularisation ...
... diving portal Blood-brain barrier Blood-ocular barrier Blood-retinal barrier Blood-testis barrier Blood-thymus barrier ... The blood-air barrier (alveolar-capillary barrier or membrane) exists in the gas exchanging region of the lungs. It exists to ... The barrier is permeable to molecular oxygen, carbon dioxide, carbon monoxide and many other gases. This blood gas barrier is ... Possible consequences of rupture of the blood-air barrier include arterial gas embolism and hemoptysis. Failure of the barrier ...
Blood-air barrier Blood-brain barrier Blood-ocular barrier Blood-testis barrier Blood-thymus barrier Biologyonline.org. Blood- ... The blood retinal barrier has two components: the retinal vascular endothelium and the retinal pigment epithelium. Retinal ... The blood-retinal barrier, or the BRB, is part of the blood-ocular barrier that consists of cells that are joined tightly ... retinal barrier. Retrieved on July 19, 2007. Vinores, SA (1995). "Assessment of blood-retinal barrier integrity". Histology and ...
Blood-air barrier Blood-brain barrier Blood-ocular barrier Blood-retinal barrier Blood-testis barrier. ... The blood-thymus barrier regulates exchange of substances between the circulatory system and thymus, providing a sequestered ... The barrier is formed by the continuous blood capillaries in the thymic cortex, reinforced by epithelial reticular cells and ... The barrier also prevents the immature T cells from contacting foreign antigens (since contact with antigens at this stage will ...
Blood-air barrier Blood-ocular barrier Blood-retinal barrier Blood-testis barrier Blood-thymus barrier Choroid plexus for blood ... The blood-brain barrier (BBB) is a highly selective semipermeable membrane barrier that separates the circulating blood from ... "History of Blood-Brain Barrier". Davis Lab. Retrieved 5 January 2015. "History of Blood-Brain Barrier". The Davis Lab. ... A few regions in the brain, including the circumventricular organs, do not have a blood-brain barrier. The blood-brain barrier ...
Blood-air barrier Blood-brain barrier Blood-ocular barrier Blood-retinal barrier Blood-thymus barrier Spermatogenesis Ganong. ... The name "blood-testis barrier" is misleading in that it is not a blood-organ barrier in a strict sense, but is formed between ... The blood-testis barrier is a physical barrier between the blood vessels and the seminiferous tubules of the animal testes. ... This composition is maintained by blood-testis barrier. The barrier also protects the germ cells from blood-borne noxious ...
Blood-air barrier Blood-brain barrier Blood-retinal barrier Blood-testis barrier Blood-thymus barrier Peiffer, Robert L.; ... Blood-retinal barrier: non-fenestrated capillaries of the retinal circulation and tight-junctions between retinal epithelial ... The blood-ocular barrier is a barrier created by endothelium of capillaries of the retina and iris, ciliary epithelium and ... As the inflammation subsides, this barrier usually returns. It consists of the following components: Blood-aqueous barrier: the ...
... dysfunction of the blood-retinal barrier, which protects the retina from many substances in the blood (including toxins and ... Narrowing or blocked retinal blood vessels can be seen clearly and this is called retinal ischemia (lack of blood flow). ... leading to the leaking of blood constituents into the retinal neuropile. Later, the basement membrane of the retinal blood ... Small blood vessels - such as those in the eye - are especially vulnerable to poor blood sugar (blood glucose) control. An ...
Two experimental treatments for retinal problems include a cybernetic replacement and transplant of fetal retinal cells.[71] ... Sack RL, Lewy AJ, Blood ML, Keith LD, Nakagawa H (July 1992). "Circadian rhythm abnormalities in totally blind people: ... However, many people are uncomfortable with communicating with the blind, and this can cause communication barriers. One of the ... That is, diabetic retinopathy describes the retinal and vitreous hemorrhages or retinal capillary blockage caused by the ...
... junctions of retinal capillary endothelial cells to prevent the free diffusion of substances between the circulating blood and ... The inner blood-retinal barrier (inner BRB) forms complex tight ... Inner blood-retinal barrier GLUT1 in long-term diabetic rats: ... The inner blood-retinal barrier (inner BRB) forms complex tight junctions of retinal capillary endothelial cells to prevent the ... 5. Alm A and Törnquist P. Lactate transport through the blood-retinal and the blood-brain barrier in rats. Ophthalmic Res 1985; ...
Researchers in Barcelona have developed a microfluidic chip that mimics the human blood-retinal barrier. The device contains ... Microfluidic Device Mimics the Blood-Retinal Barrier. January 26th, 2018 Conn Hastings Genetics, Ophthalmology ... The team plans to use the compact device to investigate the effects of various molecules on the blood-retinal barrier, to see ... The chip is designed as a more accurate representation of the physiological conditions at the blood-retinal barrier, compared ...
The retinal vessels have two barriers: the retinal pigment epithelium and the retinal vascular endothelium. Each barrier ... on Blood Retinal Barrier Breakdown. Yasuo Yanagi Department of Ophthalmology, School of Medicine, University of Tokyo, 7-3-1 ... This condition is referred to as blood retinal barrier (BRB) breakdown. Clinically, the most frequently encountered condition ... inhibits diabetes-induced retinal leukostasis and leakage, playing an important role in the pathogenesis of diabetic ...
Blood-air barrier Blood-brain barrier Blood-ocular barrier Blood-testis barrier Blood-thymus barrier Biologyonline.org. Blood- ... The blood retinal barrier has two components: the retinal vascular endothelium and the retinal pigment epithelium. Retinal ... The blood-retinal barrier, or the BRB, is part of the blood-ocular barrier that consists of cells that are joined tightly ... retinal barrier. Retrieved on July 19, 2007. Vinores, SA (1995). "Assessment of blood-retinal barrier integrity". Histology and ...
The eye possesses a similar barrier which is involved in regulating the environment of the... ... the properties of the blood-brain barrier have been the object of many investigations. ... Shiose V: Electron microscopic studies on blood-retinal and blood-aquous barriers. Jap J Ophthal 14: 73-87, 1970.Google Scholar ... This epithelium constitutes the other part of the blood-retinal barrier.. Keywords. Retinal Pigment Epithelium Capillary Wall ...
... quantify vasculopathy and blood-retinal barrier (BRB) leakage 2. measure b... ... 1. quantify vasculopathy and blood-retinal barrier (BRB) leakage. 2. measure blood-. brain barrier (BBB) permeability and ... Blood-retinal Barrier Imaging and Neuropsychiatric Sequela in Type 2 Diabetes Mellitus. 2014-08-27 03:14:27 , BioPortfolio ... Home » Topics » Top five promising drugs Phase I (February 2014) » Research » Blood-retinal Barrier Imaging and ...
The relation between expression of vascular endothelial growth factor and breakdown of the blood-retinal barrier in diabetic ... and the breakdown of the blood-retinal barrier (BRB) was investigated. VEGF mRNA expression was examined by in situ ... Because VEGF promotes endothelial proliferation, these findings suggest that VEGF plays a role in the budding of retinal ... the retinal pigment epithelium. In diabetic retinas, BRB breakdown was immunohistochemically detected, and VEGF protein ...
The outer blood retinal barrier, which is composed of the retinal pigment epithelium (RPE) and its underlying vascular support ... Developing Tissue Mimetics of the Outer Retinal Blood Barrier Project Collaborators:. Dr. Regine Choe, Dr. Jinjiang Pang, Dr. ... URMC / Labs / Benoit Lab / Projects / Developing Tissue Mimetics of the Outer Retinal Blood Barrier ... To improve the mimetic, our aims are to 1) Develop tissue mimetics of the outer retinal blood barrier through (A) biochemical ...
Characterization of Early Stages of Diabetic Retinopathy: Importance of the Breakdown of the Blood-Retinal Barrier. ... Characterization of Early Stages of Diabetic Retinopathy: Importance of the Breakdown of the Blood-Retinal Barrier ... Characterization of Early Stages of Diabetic Retinopathy: Importance of the Breakdown of the Blood-Retinal Barrier ... Characterization of Early Stages of Diabetic Retinopathy: Importance of the Breakdown of the Blood-Retinal Barrier ...
The device contains living cells and mimics the structure and physiological conditions of the blood-retinal barrier; it also ... Scientists emulate human blood-retinal barrier on a microfluidic chip The device contains living cells and mimics the structure ... and retinal pigmented epithelial cells, which form the outer layer of the blood-retinal barrier. ... A team of scientists in Barcelona has developed a microfluidic device which mimics the human blood-retinal barrier. The ...
Alpha-Mangostin Attenuation of Hyperglycemia-Induced Ocular Hypoperfusion and Blood Retinal Barrier Leakage in the Early Stage ... "Alpha-Mangostin Attenuation of Hyperglycemia-Induced Ocular Hypoperfusion and Blood Retinal Barrier Leakage in the Early Stage ...
... we have used the device to mimic the structure of the blood-retinal barrier by co-culturing primary human retinal endothelial ... microfluidic chip with crisscross microgrooves and electrophysiological electrodes for modeling the blood-retinal barrier ... microfluidic chip with crisscross microgrooves and electrophysiological electrodes for modeling the blood-retinal barrier J. ... Cell barrier formations were assessed by a permeability assay, TEER measurements, and ZO-1 expression. These results validate ...
N P Blair, M O Tso, J T Dodge; Pathologic studies of the blood--retinal barrier in the spontaneously diabetic BB rat.. Invest. ... Pathologic studies of the blood--retinal barrier in the spontaneously diabetic BB rat. ... Pathologic studies of the blood--retinal barrier in the spontaneously diabetic BB rat. ... changes of diabetic retinopathy and may provide a pathogenetic mechanism for early disruption of the blood-retinal barrier. ...
The blood-retinal barrier in chloroquine retinopathy.. Ultrastructure of blood-retinal barrier permeability in rat phototoxic ... Plasticity of the blood-retinal barrier in disease. You will receive an email whenever this article is corrected, updated, or ... Plasticity of the blood-retinal barrier in disease.. Invest. Ophthalmol. Vis. Sci. 1984;25(9):1027-1034. ... Permeability of abnormal blood-retinal barriers in rat phototoxic retinopathy: a clinicopathologic correlation study using ...
Purpose: In our previous work, we have demonstrated that the blood-retinal barrier (BRB) is established in zebrafish at 3 days ... Retinoic acid signaling has an important role in development and maintenance of the blood retinal barrier ... Retinoic acid signaling has an important role in development and maintenance of the blood retinal barrier ... Retinoic acid signaling has an important role in development and maintenance of the blood retinal barrier. Invest. Ophthalmol. ...
Tout S Chan-Ling T Hollander H Stone J . The role of Muller cells in the formation of the blood-retinal barrier. Neuroscience. ... The highly similar retinal vascular phenotypes of Ndp and Fzd4 knockout mice suggest that Norrins effects during retinal blood ... Frizzled 4 Is Required for Retinal Angiogenesis and Maintenance of the Blood-Retina Barrier ... Frizzled 4 Is Required for Retinal Angiogenesis and Maintenance of the Blood-Retina Barrier ...
The present study is an exploratory investigation of blood-retinal barrier permeability, retinal thickness, and retinal vessel ... Progression of Diabetic Macular Edema: Correlation with Blood-Retinal Barrier Permeability, Retinal Thickness, and Retinal ... Progression of Diabetic Macular Edema: Correlation with Blood-Retinal Barrier Permeability, Retinal Thickness, and Retinal ... mean blood pressure, blood-retinal barrier permeability, retinal thickness, and vessel diameters. The Cox model includes the ...
We showed that cells lining the blood-retinal barrier (BRB), the retinal endothelium, and retinal pigment epithelium (RPE) were ... Zika virus infects cells lining the blood-retinal barrier and causes chorioretinal atrophy in mouse eyes. ... Zika virus infects cells lining the blood-retinal barrier and causes chorioretinal atrophy in mouse eyes. ... Human primary retinal pigment epithelial cells (Pr. RPE), the immortal RPE cell line (ARPE-19), primary retinal vascular ...
VEGF-initiated blood-retinal barrier breakdown in early diabetes. Invest Ophthalmol Vis Sci. 2001; 42: 2408-2413. ... Diabetes-induced superoxide anion and breakdown of the blood-retinal barrier: role of the VEGF/uPAR pathway. PLoS One. 2013; 8 ... In situ kinetics of glucose transport across the blood-retinal barrier in normal rats and rats with streptozocin-induced ... Molecular basis of the inner blood-retinal barrier and its breakdown in diabetic macular edema and other pathological ...
The retinal pigment epithelial layer constitutes outer blood retinal barrier (BRB) that lies between retina and leaky choroidal ... Disruption of outer blood retinal barrier by Toxoplasma gondii-infected monocytes is mediated via FAK signaling pathway ... Disruption of outer blood retinal barrier by Toxoplasma gondii-infected monocytes is mediated via FAK signaling pathway ... Disruption of outer blood retinal barrier by Toxoplasma gondii-infected monocytes is mediated via FAK signaling pathway. Invest ...
In Vivo Model of the Molecular, Functional, and Morphological Changes Occurring During Blood Retinal Barrier Disruption by VEGF ... In Vivo Model of the Molecular, Functional, and Morphological Changes Occurring During Blood Retinal Barrier Disruption by VEGF ... there is need for in vivo models that are amenable to functional and molecular analysis during blood-retinal barrier (BRB) ... and Morphological Changes Occurring During Blood Retinal Barrier Disruption by VEGF. Invest. Ophthalmol. Vis. Sci. 2014;55(13): ...
blood-retinal barrier (BRB). vitreous fluorophotometry. vascular endothelium. HPLC. smoking. nicotine. cotinine. CCR. ... Background The aim of the study was the fluorophotometric evaluation of the blood-retinal barrier (BRB) integrity in smoking ... Background The aim of the study was the fluorophotometric evaluation of the blood-retinal barrier (BRB) integrity in smoking ... The Influence of Arterial Hypertension and Smoking on Blood-Retinal Barrier. Arkadiusz Pogrzebielski, Wojciech Lubaszewski, ...
The purpose of this study was to develop and characterize a quantitative assay of blood-retinal barrier (BRB) function in mice ... The purpose of this study was to develop and characterize a quantitative assay of blood-retinal barrier (BRB) function in mice ... The purpose of this study was to develop and characterize a quantitative assay of blood-retinal barrier (BRB) function in mice ... The purpose of this study was to develop and characterize a quantitative assay of blood-retinal barrier (BRB) function in mice ...
Blood-retinal barrier in hypoxic ischaemic conditions: Basic concepts, clinical features and management. Progress in Retinal ... The blood-retinal barrier (BRB) plays an important role in the homeostatic regulation of the microenvironment in the retina. It ... Blood-retinal barrier in hypoxic ischaemic conditions: Basic concepts, clinical features and management. ... being formed by the tight junctions between neighbouring retinal capillary endothelial cells and the outer barrier (oBRB) by ...
Luna, J. D., Chan, C. C., Derevjanik, N. L., Mahlow, J., Chiu, C., Peng, B., ... Vinores, S. A. (1997). Blood-retinal barrier ( ... T1 - Blood-retinal barrier (BRB) breakdown in experimental autoimmune uveoretinitis. T2 - Comparison with vascular endothelial ... Blood-retinal barrier (BRB) breakdown in experimental autoimmune uveoretinitis: Comparison with vascular endothelial growth ... Blood-retinal barrier (BRB) breakdown in experimental autoimmune uveoretinitis: Comparison with vascular endothelial growth ...
  • TUNEL and brain-specific homeobox/POU domain protein 3A (BRN3A) markers were used to examine retinal ganglion cells. (springer.com)
  • Lomerizine also shows neuroprotective effects against secondary degeneration resulting from injury in retinal ganglion cells. (wikipedia.org)
  • citation needed] His lab also discovered and developed methods for the purification and culturing of retinal ganglion cells and the glial cells in which they interact, including the oligodendrocytes and astrocytes of the optic nerve. (wikipedia.org)
  • Biological support for the role of inflammation in early diabetes is the adhesion of leukocytes to the retinal vasculature (leukostasis) observed in diabetic retinopathy. (hindawi.com)
  • The choroid plexus (CP), main component of blood-cerebrospinal fluid barrier (BCSFB), protects the brain from peripheral inflammation similar to the blood-brain barrier. (bioportfolio.com)
  • The device is a relatively simple, passive cell-sorter that Karnik says may efficiently sort out material such as white blood cells-cells that may quickly be counted to identify conditions such as sepsis and inflammation. (medicalxpress.com)
  • In conclusion, the results suggest that the retinal protective effects of ZZRext occur through improved retinal structural change and inhibiting retinal inflammation. (mdpi.com)
  • Liu, I.-M. Consumption of Polyphenol-Rich Zingiber Zerumbet Rhizome Extracts Protects against the Breakdown of the Blood-Retinal Barrier and Retinal Inflammation Induced by Diabetes. (mdpi.com)
  • In conclusion, treatment of diabetic rats with zerumbone attenuates the severity of retinal inflammation and angiogenesis, via inhibition of p38 MAPK and NF-κB signaling pathways. (mdpi.com)
  • Expression of biomarkers for retinal inflammation was assessed by immunoblotting of TNF-α, ICAM-1, and NF-κB. (diabetesjournals.org)
  • Retinal inflammation is playing a crucial role in the development of DR, and targeting inflammatory mediators is a promising strategy for controlling DR. Here, we investigated compound Chinese medicine Luo Tong formula (LTF) alleviated retinal inflammatory responses in a STZ-induced diabetic rat model. (springer.com)
  • The defective intestinal epithelial tight junction (TJ) barrier has been postulated to be an important pathogenic factor contributing to intestinal inflammation. (jimmunol.org)
  • Additionally, pharmacologic enhancement of intestinal TJ barrier with AT-1001 (a zonulin peptide inhibitor) prevented the development of intestinal inflammation in IL-10 −/− mice, suggesting that the defective intestinal TJ barrier was necessary for the development of intestinal inflammation ( 1 ). (jimmunol.org)
  • Inflammation can break down this barrier allowing drugs and large molecules to penetrate into the eye. (wikipedia.org)
  • As the inflammation subsides, this barrier usually returns. (wikipedia.org)
  • Therefore, if blood, cells or other byproducts of inflammation get into the vitreous, they will remain there unless removed surgically. (wikipedia.org)
  • They believe that these changes eventually alter the functioning of the blood-brain barrier, causing brain inflammation. (wikipedia.org)
  • Menkes disease (Menkes kinky hair syndrome) (rare - UK incidence 1/100,000) Copper deficiency Aceruloplasminemia Greater-than-normal ceruloplasmin levels may indicate or be noticed in: copper toxicity / zinc deficiency pregnancy oral contraceptive pill use lymphoma acute and chronic inflammation (it is an acute-phase reactant) rheumatoid arthritis Angina Alzheimer's disease Schizophrenia Obsessive-compulsive disorder Normal blood concentration of ceruloplasmin in humans is 20-50 mg/dL. (wikipedia.org)
  • GM atrophy is independent of the MS lesions and is associated with physical disability, fatigue, and cognitive impairment in MS At least five characteristics are present in CNS tissues of MS patients: Inflammation beyond classical white matter lesions, intrathecal Ig production with oligoclonal bands, an environment fostering immune cell persistence, Follicle-like aggregates in the meninges and a disruption of the blood-brain barrier also outside of active lesions. (wikipedia.org)
  • At least five characteristics are present in CNS tissues of MS patients: Inflammation beyond classical white matter lesions (NAWM, NAGM), intrathecal Ig production with oligoclonal bands, an environment fostering immune cell persistence, Follicle-like aggregates in the meninges (B-cells mostly infected with EBV) and a disruption of the blood-brain barrier even outside of active lesions. (wikipedia.org)
  • Here we will summarize the effects of hyperglycemia-induced O-GlcNAc modification on the retinal neurovasculature in a cell-specific manner, providing new insight into the role of O-GlcNAc modification in early loss of retinal pericytes and the pathogenesis of DR. (clinsci.org)
  • If mice are given 9-cis -retinal to counter the loss of retinal isomerase, the P1 wave is partially restored. (nature.com)
  • The potential mechanisms linking retinal neurodegeneration and early microvascular impairment, and the effects of neuroprotective drugs are summarised. (springer.com)
  • Despite this intricate relationship, retinal neurodegeneration is a critical endpoint and neuroprotection, itself, can be considered a therapeutic target, independently of its potential impact on microvascular disease. (springer.com)
  • Sphingosine-1-phosphate protects against brain microvascular endothelial junctional protein disorganization and barrier dysfunction caused by alcohol. (bioportfolio.com)
  • It is widely accepted that the visual impairment of diabetic patients results from retinal microvascular changes. (springer.com)
  • Hypertensive heart disease is the result of structural and functional adaptations leading to left ventricular hypertrophy, diastolic dysfunction, CHF, abnormalities of blood flow due to atherosclerotic coronary artery disease and microvascular disease, and cardiac arrhythmias. (wikipedia.org)
  • Previous investigations have demonstrated that the blood-retinal barrier excludes large molecules, such as horseradish peroxidase (1,2) and microperoxidase (3) and even the low molecular weight compound, fluorescein (4) from entering the retinal tissue. (springer.com)
  • Background The aim of the study was the fluorophotometric evaluation of the blood-retinal barrier (BRB) integrity in smoking and non-smoking patients with arterial hypertension without signs of BRB breakdown in form retinal hemorrhages, hard and soft exudates seen during ophthalmoscopy and fluorescein angiography. (viamedica.pl)
  • Retinal delivery of sodium fluorescein, budesonide & celecoxib following subconjunctival injection. (springer.com)
  • The chip is designed as a more accurate representation of the physiological conditions at the blood-retinal barrier, compared with conventional tissue culture flasks. (medgadget.com)
  • To improve the mimetic, our aims are to 1) Develop tissue mimetics of the outer retinal blood barrier through (A) biochemical modification and (B) spatially organized culture of hiPSC-RPE and hiPSC-derived vascular networks enabled by PEG hydrogels and 2) Evaluate structure and function of RPE-CC tissue mimetics compared to in vivo tissue. (rochester.edu)
  • In the figure to the right, retinal barrier tissue mimetics exhibit morphological and functional similarities to native RPE. (rochester.edu)
  • Whilst these findings do not provide a complete picture of VEGFA signalling in the microvasculature-there are still unclear roles for heterodimeric receptor complexes as well as co-receptors-they provide essential insight into the adaptation of vascular systems to environmental cues that are naturally different, depending on whether they are present on the blood or tissue side. (mdpi.com)
  • Localized reduction of blood flow to brain tissue due to arterial obstruction or systemic hypoperfusion. (bioportfolio.com)
  • This paradigm involves a series of adhesion molecules that act in an interdependent fashion to allow fast flowing cells in the mainstream of blood to leave the circulation and enter the adjacent tissue. (jimmunol.org)
  • Healthy growth of tissue cells aid in maintaining a moist environment within the urinary, respiratory, genital, intestinal tracts and eyes, mouth and stomach linings, primarily acting as a barrier against harmful bacteria and virus's (Deen & Hark, 2007). (wikipedia.org)
  • Transcrocetinate sodium has shown promise of effectiveness in restoring tissue oxygen levels and improving the ability to walk in a clinical trial of patients with peripheral artery disease (PAD) in which reduced delivery of oxygen-rich blood to tissues can cause severe leg pain and impair mobility. (wikipedia.org)
  • They perform many functions, including biochemical support of endothelial cells that form the blood-brain barrier, provision of nutrients to the nervous tissue, maintenance of extracellular ion balance, and a role in the repair and scarring process of the brain and spinal cord following traumatic injuries. (wikipedia.org)
  • It has two functionally distinct membranes that face different extracellular environments: the apical (retinal-facing) membrane directly opposes the photoreceptor outer segments, and the basolateral (serosal-facing) membrane faces the fenestrated choroicapillaris. (jneurosci.org)
  • The progenitor cell can then divide and differentiate into a number of retinal cell types, including photoreceptor cells, that may have been damaged during injury. (wikipedia.org)
  • At blood-neural barriers, endothelial VEGFA signalling is highly polarised, with entirely different responses being triggered by luminal or abluminal stimulation. (mdpi.com)
  • In The Blood-Brain and Other Neural Barriers: Reviews and Protocols, experts in the field present a series of cutting-edge protocols which can be used to study the barriers. (springer.com)
  • More recently, the function of astrocytes has been reconsidered, and they are now thought to play a number of active roles in the brain, including the secretion or absorption of neural transmitters and maintenance of the blood-brain barrier. (wikipedia.org)
  • These data indicate the presence of metabotropic P 2Y /P 2U -purinoceptors at the RPE apical membrane and implicate extracellular ATP in vivo as a retinal signaling molecule that could help regulate the hydration and chemical composition of the subretinal space. (jneurosci.org)
  • The blood-brain barrier (BBB) is a highly selective semipermeable membrane barrier that separates the circulating blood from the brain and extracellular fluid in the central nervous system (CNS). (wikipedia.org)
  • This barrier also includes a thick basement membrane and astrocytic endfeet. (wikipedia.org)
  • The blood-air barrier (alveolar-capillary barrier or membrane) exists in the gas exchanging region of the lungs. (wikipedia.org)
  • Taurine crosses the blood-brain barrier and has been implicated in a wide array of physiological phenomena including inhibitory neurotransmission, long-term potentiation in the striatum/hippocampus, membrane stabilization,[unreliable medical source? (wikipedia.org)
  • One of the biggest barriers to treating ALS is that its progression is dynamic-many different cell types and mechanisms are involved-so treating it at one stage of the disease might have very different, and potentially harmful, consequences at a different stage," said Tom Maniatis, PhD, a principal investigator at Columbia's Mortimer B. Zuckerman Mind Brain Behavior Institute and the study's senior author. (medicalxpress.com)
  • In the initial, vasoconstrictive stage, there is vasospasm and an increase in retinal arteriolar tone owing to local autoregulatory mechanisms. (wikipedia.org)
  • Mechanisms of low ceruloplasmin levels: Gene expression genetically low (aceruloplasminemia) Copper levels are low in general Malnutrition/trace metal deficiency in the food source Copper does not cross the intestinal barrier due to ATP7A deficiency (Menkes disease) Delivery of copper into the lumen of the ER-Golgi network is absent in hepatocytes due to absent ATP7B (Wilson's disease) Copper availability doesn't affect the translation of the nascent protein. (wikipedia.org)
  • However, retinal neurodegeneration is already present before any microcirculatory abnormalities can be detected in ophthalmoscopic examination. (nih.gov)
  • The authors present the case of a patient with Waldenstrom macroglobulinemia who developed dramatic retinal architecture abnormalities after a prolonged period of sustained elevated IgM levels. (lww.com)
  • Reactive astrogliosis is the most common form of gliosis and involves the proliferation of astrocytes, a type of glial cell responsible for maintaining extracellular ion and neurotransmitter concentrations, modulating synapse function, and forming the blood-brain barrier. (wikipedia.org)