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Retinal Tissue (retinal + tissue)
Selected AbstractsComplete reconstruction of the retinal laminar structure from a cultured retinal pigment epithelium is triggered by altered tissue interaction and promoted by overlaid extracellular matricesDEVELOPMENTAL NEUROBIOLOGY, Issue 14 2009Fusako Kuriyama Abstract The retina regenerates from retinal pigment epithelial (RPE) cells by transdifferentiation in the adult newt and Xenopus laevis when it is surgically removed. This was studied under a novel culture condition, and we succeeded, for the first time, in developing a complete retinal laminar structure from a single epithelial sheet of RPE. We cultured a Xenopus RPE monolayer sheet isolated from the choroid on a filter cup with gels overlaid and found that the retinal tissue structure differentiated with all retinal layers present. In the culture, RPE cells isolated themselves from the culture substratum (filter membrane), migrated, and reattached to the overlaid gel, on which they initiated transdifferentiation. This was exactly the same as observed during in vivo retina regeneration of X. laevis. In contrast, when RPE monolayers were cultured similarly without isolation from the choroid, RPE cells proliferated, but remained pigmented instead of transdifferentiating, indicating that alteration in tissue interaction triggers transdifferentiation. We then examined under the conventional tissue culture condition whether altered RPE-choroid interaction induces Pax6 expression. Pax6 was upregulated in RPE cells soon after they were removed from the choroid, and this expression was not dependent of FGF2. FGF2 administration was needed for RPE cells to maintain Pax6 expression. From the present results, in addition to our previous ones, we propose a two-step mechanism of transdifferentiation: the first step is a reversible process and is initiated by the alteration of the cell-extracellular matrix and/or cell,cell interaction followed by Pax6 upregulation. FGF2 plays a key role in driving RPE cells into the second step, during which they differentiate into retinal stem cells. © 2009 Wiley Periodicals, Inc. Develop Neurobiol, 2009 [source] Ganglion cell regeneration following whole-retina destruction in zebrafishDEVELOPMENTAL NEUROBIOLOGY, Issue 2 2008Tshering Sherpa Abstract The retinas of adult teleost fish can regenerate neurons following injury. The current study provides the first documentation of functional whole retina regeneration in the zebrafish, Danio rerio, following intraocular injection of the cytotoxin, ouabain. Loss and replacement of laminated retinal tissue was monitored by analysis of cell death and cell proliferation, and by analysis of retina-specific gene expression patterns. The spatiotemporal process of retinal ganglion cell (RGC) regeneration was followed through the use of selective markers, and was found to largely recapitulate the spatiotemporal process of embryonic ganglion cell neurogenesis, over a more protracted time frame. However, the re-expression of some ganglion cell markers was not observed. The growth and pathfinding of ganglion cell axons was evaluated by measurement of the optic nerve head (ONH), and the restoration of normal ONH size was found to correspond to the time of recovery of two visually-mediated behaviors. However, some abnormalities were noted, including overproduction of RGCs, and progressive and excessive growth of the ONH at longer recovery times. This model system for whole-retina regeneration has provided an informative view of the regenerative process. © 2007 Wiley Periodicals, Inc. Develop Neurobiol, 2008 [source] Differentiation-dependent sensitivity to cell death induced in the developing retina by inhibitors of the ubiquitin-proteasome proteolytic pathwayEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 10 2001D. D. C. Neves Abstract The effects of inhibitors of proteasome function were studied in the retina of developing rats. Explants from the retina of neonatal rats at postnatal day (P) 3 or P6 were incubated with various combinations of the proteasome inhibitor carbobenzoxyl-leucinyl-leucinyl-leucinal (MG132), the protein synthesis inhibitor anisomycin, or the adenylyl cyclase activator forskolin. MG132 induced cell death in a subset of cells within the neuroblastic (proliferative) layer of the retinal tissue. The cells sensitive to degeneration induced by either MG132 or anisomycin, were birthdated by bromodeoxyuridine injections. This showed that the MG132-sensitive population includes both proliferating cells most likely in their last round of cell division, and postmitotic undifferentiated cells, at a slightly earlier stage than the population, sensitive to anisomycin-induced cell death. The results show that sensitivity to cell death induced by proteasome inhibitors defines a window of development in the transition from the cell cycle to the differentiated state in retinal cells. [source] Gelatin-based biomimetic tissue adhesive.JOURNAL OF BIOMEDICAL MATERIALS RESEARCH, Issue 2 2006Potential for retinal reattachment Abstract An adhesive that cures under moist/wet conditions could facilitate surgical procedures for retinal reattachment. We are investigating an adhesive that mimics the factor XIIIa-mediated crosslinking of fibrin that occurs in the late stages of the blood coagulation cascade. Specifically, we use gelatin as the structural protein (in place of fibrin), and crosslink gelatin using a calcium-independent microbial transglutaminase (in place of the calcium-dependent transglutaminase factor XIIIa). Injection of gelatin and microbial transglutaminase (mTG) into the vitreous cavity of Sprague Dawley white rats did not elicit structural or cellular damage to the retina as evidenced from histological evaluation 2 weeks post-injection. Qualitative in vitro studies indicate that the gelatin,mTG adhesive binds to bovine retinal tissue under wet conditions. Quantitative lap-shear tests were performed with more robust bovine tissue from the choroid and sclera. The lap-shear strength of the biomimetic gelatin,mTG adhesive was independent of tissue-type and ranged from 15 to 45 kPa, which is comparable to the values reported for other soft-tissue adhesives. These studies suggest that the mTG-crosslinked gelatin may provide a simple, safe, and effective adhesive for ophthalmic applications. © 2005 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 2006 [source] Glutamate and nitric oxide modulate ERK and CREB phosphorylation in the avian retina: evidence for direct signaling from neurons to Müller glial cellsJOURNAL OF NEUROCHEMISTRY, Issue 2 2009Renato Esteves da Silva Socodato Abstract Glutamate signaling in the mature retinal tissue is very important for accurate sensory decoding by retinal neurons and orchestrates the fine-tuned output from the retina to higher-order centers at the cerebral cortex. In this study, we show that glutamate induces a rapid extracellular-regulated kinase and cAMP-responsive element binding protein (CREB) phosphorylation in cultured developing retinal neurons. This process is reliant on ,-amino-3-hydroxy-5-methylisoxazole-4-propionate receptors and nitric oxide (NO) signaling and independent of NMDA receptors activation, as it is blocked by ,-amino-3-hydroxy-5-methylisoxazole-4-propionate/kainate antagonists as well as inhibiting NO synthase with NG-nitro- l -arginine methyl ester but not by the NMDA channel blocker dizocilpine maleate. The effect of NO on extracellular-regulated kinase and CREB is mediated by the classical NO/soluble guanylyl cyclase/protein kinase G pathways as it is inhibited by the soluble guanylyl cyclase blocker 1H-[1,2,4]oxadiazole[4,3-a]quinoxalin-1-one and the protein kinase G inhibitor KT5823, respectively. Immunocytochemical data suggest that increased CREB phosphorylation in response to glutamate occurs in glial cell nuclei. We also have supporting evidence suggesting that neuronally produced NO directly reaches the glial cells and stimulates CREB phosphorylation. Hence, the results indicate the importance of neuronal,glial communication and glutamate/NO/CREB linkage during retinal development. [source] 3123: Non-invasive measurement of retinal oxygenation: principles and expectationsACTA OPHTHALMOLOGICA, Issue 2010M HAMMER Purpose To determine oxygen saturation (SO2) of blood inside retinal vessels which is an essential measure for the estimation of oxygen supply to the tissue as well as its oxygen consumption. Methods Two-, four-, and multiple - wavelength approaches to the non-invasive measurement of SO2 will be discussed. The dual wavelength technique, imaging the fundus at 548 and 610 nm, showed to be most appropriate for clinical routine investigations. The SO2 of the hemoglobin in retinal arterioles and venules is calculated from the ratio of the optical densities of the vessels at both wavelengths. Results From a healthy control population, mean arterial and venous SO2 were measured to be 98±10.1% and 65±11.7% with reproducibility of 2.52% and 3.25% respectively. In a cohort of 41 patients (mean age: 65±12.3 years) with diabetic retinopathy (DR), we found an increase of the venous SO2 with the severity of DR: Mild non-proliferative DR 69±7%, moderate non-proliferative DR 70±5%, severe non-proliferative DR, 75±5%, and proliferative DR 75±8%. Measurements of SO2 in accordance with vessel diameters revealed a correlation of the venous SO2 with arterial as well as venous diameters in 159 diabetic patients (mean age: 55.8±13.9 years) with no or non , proliferative DR. Increased venous SO2 is an indicator of insufficient oxygen supply to the retinal tissue. The correlation of the vessel diameters with venous SO2 may point to compensatory mechanisms of retinal blood flow regulation. Conclusion Accurate retinal vessel oximetry is possible by non , invasive optical methods. Combined with measurements characterising the retinal blood flow, it is a powerful tool for the estimation of retinal oxygen supply and consumption. Commercial interest [source] 4144: Retinal blood vessel phenotyping in miceACTA OPHTHALMOLOGICA, Issue 2010J RUBERTE Purpose In the retina there is a compromise between optimal visual function and optimal oxygenation. Retinal blood vessels have a relative sparse distribution and their size is small in order to minimise optical interference with the light path. Hence, the blood flow volume in the retina is relatively low. This fact, together with the high oxygen consumption of the retinal tissue, could facilitate the development of retinal hypoxia and subsequent retinopathy when the vascular bed is altered. Thus, the analysis of retinal blood vessel must be a crucial step during retinal phenotyping in mutant mice. Methods Different technologies and methods have been used in order to analyze structure, distribution and function of retinal blood vessels, among others: retinal digest preparations, retinal whole mount immunohistochemistry, transmission and scanning electron microscopy, fluorescein and Mercox vascular injections and scanner laser ophthalmoscopy. Results In our laboratory, morphological and topographic alterations of retinal blood vessels in Bmi1 and Sirt1 knockout mice, as well as in IGF-1 and IL-10 transgenic mice, have been observed and documented Conclusion The mouse genome is fully sequenced. 99% of the coding genes present in man are also present in mouse. Moreover, the majority of disease-related genes have been conserved since the emergence of the bony fishes about 400 million years ago. These facts and the development during the last two decades of an extensive toolbox to study the functional effects of genetic variation in mice, make them the ideal model organism for the study of human eye diseases. In this sense, morphological and functional analyses of retinal blood vessel in mutant mice could help to understand vascular gene-based mechanisms that lead to retinopathy [source] Retinal oxygenation in diabetic retinopathyACTA OPHTHALMOLOGICA, Issue 2009SH HARDARSON Purpose Diabetic retinopathy (DR) is believed to cause retinal tissue hypoxia by damaging retinal capillaries. The purpose of this study was to examine the effect of diabetic retinopathy on oxygen saturation in retinal arterioles and venules. Methods The retinal oximeter (Oxymap ehf., Reykjavik, Iceland) is composed of a fundus camera, beam splitter and light filters. Specialized software calculates relative oxygen saturation from light absorption at two wavelengths of light (605nm and 586nm). One first or second degree temporal arteriole and venule were measured in one eye of 31 healthy individual and 28 patients with diabetic retinopathy. The diabetic patients had background DR (n=6), macular oedema (n=7), untreated preproliferative or proliferative DR (n=7) or stable proliferative DR after treatment (n=8). Statistical analyses were performed with an unpaired t-test, one-way ANOVA and Dunnett's post test. Results Retinal arteriolar saturation was 93±4% (n=31, mean±SD) in healthy subjects and 101±6% (n=28) in patients with DR (p<0.0001). Retinal venular saturation was 58±6% in healthy subjects and 67±8% in diabetic patients (p<0.0001). Arteriolar and venular saturation was higher in all subgroups of diabetic patients (see methods) than in healthy subjects. Conclusion Increased oxygen saturation in retinal vessels in diabetic retinopathy, also found by other researchers, is consistent with poor distribution of blood and oxygen to the retinal tissue rather than decreased total retinal blood flow. Poor distribution of oxygen may be caused by capillary dropouts and shunts as well as thickening of the capillary walls. Commercial interest [source] Treatments for choroidal and retinal neovascularization: a focus on oligonucleotide therapy and delivery for the regulation of gene functionCLINICAL & EXPERIMENTAL OPHTHALMOLOGY, Issue 1 2005Robert J Marano PhD Abstract Blinding eye diseases caused by neovascularization of the retinal tissue are the leading cause of blindness in Western societies. Current treatments, such as laser photocoagulation, are limited in their effectiveness at halting the progression of angiogenesis and are unable to reduce the number of vessels once they have developed. In addition, although complete blindness is often avoided, vision is often permanently impaired by the treatment itself. Several less invasive treatments are being developed and one of these is oligonucleotide gene therapy in which short stretches of nucleotides are being used as inhibitors of key, metabolic processes involved in angiogenesis. Combined with this is the development of new and improved nucleotide chemistries aimed at overcoming many of the problems associated with oligonucleotide gene therapy, such as poor longevity because of endonuclease activity. In addition, advancements in delivery systems have further enhanced the efficacy of oligonucleotide gene therapy by increasing cellular penetration and localizing delivery to specific cell types and organs. [source] Effect of Visible Light on Normal and P23H-3 Transgenic Rat Retinas: Characterization of a Novel Retinoic Acid Derivative Present in the P23H-3 RetinaPHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 3 2006Todd Duncan ABSTRACT Transgenic rats with the P23H mutation in rhodopsin exhibit increased susceptibility to light damage, compared with normal animals. It is known that light-induced retinal damage requires repetitive bleaching of rhodopsin and that photoreceptor cell loss is by apoptosis; however, the underlying molecular mechanism(s) leading to photoreceptor cell death are still unknown. Photoproducts, such as all- trans retinal or other retinoid metabolites, released by the extensive bleaching of rhodopsin could lead to activation of degenerative processes, especially in animals genetically predisposed to retinal degenerations. Using wild-type and transgenic rats carrying the P23H opsin mutation, we evaluated the effects of acute intense visible light on retinoid content, type and distribution in ocular tissues. Rats were exposed to green light (480,590 nm) for 0, 5, 10, 30 and 120 min. Following light treatment, rats were sacrificed and neural retinas were dissected free of the retinal pigment epithelium. Retinoids were extracted from retinal tissues and then subjected to HPLC and mass spectral analysis. We found that the light exposure affected relative levels of retinoids in the neural retina and retinal pigment epithelium of wild-type and P23H rat eyes similarly. In the P23H rat retina but not the wild-type rat retina, we found a retinoic acid-like compound with an absorbance maximum of 357 nm and a mass of 304 daltons. Production of this retinoic acid-like compound in transgenic rats is influenced by the age of the animals and the duration of light exposure. It is possible that this unique retinoid may be involved in the process of light-induced retinal degeneration. [source] | |||||||||||||