Browsing by Subject "Blood retinal barrier"

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    Assessment of blood-retina1 barrier integrity
    (Murcia : F. Hernández, 1995) Vinores, S.A.
    The blood-retina1 barrier consists of two components which are comprised of the retinal vascular endothelium and the retinal pigment epithelium, respectively. Its functional integrity can be recognized by tight junctions between these cells with a paucity of endocytic vesicles within them and the presence of the molecules that regulate the ionic and metabolic gradients that constitute the barrier. The banier is compromised in severa1 disease processes and by a variety of agents, but in most cases the location and mechanism for barrier failure is not understood. Perfusion with a variety of radiolabeled tracer molecules, vitreous fluorophotometry, or magnetic resonance imaging can be used to quantitate blood-retina1 barrier leakage. Fluorescein angiography or magnetic resonance imaging can localize sites of leakage in vivo with limited resolution. Evans blue dye can be used to visualize blood-retina1 barrier failure in gross pathological specimens and immunohistochemical labeling of serum proteins such as albumin or fibrinogen can be used to localize sites of blood-retina1 barrier breakdown by light microscopy. Tracers such as horseradish peroxidase, microperoxidase, or lanthanum, or the immunocytochemical demonstration of albumin can be used to reveal bloodretinal barrier breakdown at the ultrastructural leve1 and provide insights into the mechanisms involved. This review discusses the advantages and lirnitations of each of these methods to aid in selection of the appropriate techniques to derive the desired information.
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    Blood-retina1 barrier breakdown in retinitis pigmentosa: light and electron microscopic immunolocalization
    (Murcia : F. Hernández, 1995) Vinores, S.A.; Küchle, M.; Derevjanik, N.L.; Henderer, J.D.; Mahlow, J.; Green, W.R.; Campochiaro, P.A.
    Macular edema can contribute to visual loss in the retinitis pigmentosa (RP), but the sites and mechanism of blood-retina1 barrier (BRB) breakdown leading to macular edema are not known. An understanding of the mechanisms involved could lead to the design of effective pharmacologic therapy to prevent or minimize macular edema in RP. To investigate this problem, immunohistochemical staining for albumin was performed on paraffin sections of 22 normal and 29 RPaffected eyes. Specimens were graded for extent of albumin extravasation in different regions of the retina, optic nerve head, ciliary body, and iris. Electron microscopic immunocytochemical staining for albumin was performed on an additional 6 normal and 9 RPaffected eyes. Two-thirds of the eyes from patients with RP and no other ocular disorders demonstrated extravascular albumin in the inner portion of the posterior retina. This was evident even in the absence of cystoid macular edema (CME), but eyes that had CME showed extensive BRB failure. In some cases, passage of albumin from the choroid to the retina was prevented even in the absence of the retinal pigment epithelium (RPE). Electron microscopic immunocytochemistry revealed that albumin permeated retinal vascular endothelial cells and RPE cells that showed degenerative changes in RP.
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    MMP-3 Deficiency Alleviates Endotoxin-Induced Acute Inflammation in the Posterior Eye Segment
    (MDPI, 2016-11-01) Van Hove, Inge; Lefevere, Evy; De Groef, Lies; Sergeys, Jurgen; Libert, Claude; Vandenbroucke, Rossmarijn; Moons, Lieve; Salinas Navarro, Manuel Ángel; Anatomía Humana y Psicobiología
    Matrix metalloproteinase-3 (MMP-3) is known to mediate neuroinflammatory processes by activating microglia, disrupting blood–central nervous system barriers and supporting neutrophil influx into the brain. In addition, the posterior part of the eye, more specifically the retina, the retinal pigment epithelium (RPE) and the blood–retinal barrier, is affected upon neuroinflammation, but a role for MMP-3 during ocular inflammation remains elusive. We investigated whether MMP-3 contributes to acute inflammation in the eye using the endotoxin-induced uveitis (EIU) model. Systemic administration of lipopolysaccharide induced an increase in MMP-3 mRNA and protein expression level in the posterior part of the eye. MMP-3 deficiency or knockdown suppressed retinal leukocyte adhesion and leukocyte infiltration into the vitreous cavity in mice subjected to EIU. Moreover, retinal and RPE mRNA levels of intercellular adhesion molecule 1 (Icam1), interleukin 6 (Il6), cytokine-inducible nitrogen oxide synthase (Nos2) and tumor necrosis factor α (Tnfα), which are key molecules involved in EIU, were clearly reduced in MMP-3 deficient mice. In addition, loss of MMP-3 repressed the upregulation of the chemokines monocyte chemoattractant protein (MCP)-1 and (C-X-C motif) ligand 1 (CXCL1). These findings suggest a contribution of MMP-3 during EIU, and its potential use as a therapeutic drug target in reducing ocular inflammation.