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  1. Article: Donáth Tibor (1926–2018).

    Szél, Ágoston

    Orvosi hetilap

    2018  Volume 159, Issue 6, Page(s) 203–205

    Title translation Tibor Donáth (1926-2018).
    MeSH term(s) Anatomy/history ; Dictionaries as Topic ; History, 20th Century ; History, 21st Century ; Humans ; Hungary ; Societies, Medical
    Language Hungarian
    Publishing date 2018-02-13
    Publishing country Hungary
    Document type Biography ; Historical Article ; Journal Article
    ZDB-ID 123879-6
    ISSN 1788-6120 ; 0030-6002
    ISSN (online) 1788-6120
    ISSN 0030-6002
    DOI 10.1556/650.2018.HO2592
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Possible retinotoxicity of long-term vardenafil treatment.

    Szabó, Klaudia / Dékány, Bulcsú / Énzsöly, Anna / Hajdú, Rozina Ida / Laurik-Feuerstein, Lenke Kornélia / Szabó, Arnold / Radovits, Tamás / Mátyás, Csaba / Oláh, Attila / Kovács, Krisztián András / Szél, Ágoston / Somfai, Gábor Márk / Lukáts, Ákos

    Experimental eye research

    2024  Volume 243, Page(s) 109890

    Abstract: Phosphodiesterase (PDE) inhibitors - such as vardenafil - are used primarily for treating erectile dysfunction via increasing cyclic guanosine monophosphate (cGMP) levels. Recent studies have also demonstrated their significant cardioprotective effects ... ...

    Abstract Phosphodiesterase (PDE) inhibitors - such as vardenafil - are used primarily for treating erectile dysfunction via increasing cyclic guanosine monophosphate (cGMP) levels. Recent studies have also demonstrated their significant cardioprotective effects in several diseases, including diabetes, upon long-term, continuous application. However, PDE inhibitors are not specific for PDE5 and also inhibit the retinal isoform. A sustained rise in cGMP in photoreceptors is known to be toxic; therefore, we hypothesized that long-term vardenafil treatment might result in retinotoxicity. The hypothesis was tested in a clinically relevant animal model of type 2 diabetes mellitus. Histological experiments were performed on lean and diabetic Zucker Diabetic Fatty rats. Half of the animals were treated with vardenafil for six months, and the retinal effects were evaluated. Vardenafil treatment alleviated rod outer segment degeneration but decreased rod numbers in some positions and induced changes in the interphotoreceptor matrix, even in control animals. Vardenafil treatment decreased total retinal thickness in the control and diabetic groups and reduced the number of nuclei in the outer nuclear layer. Müller cell activation was detectable even in the vardenafil-treated control animals, and vardenafil did not improve gliosis in the diabetic group. Vardenafil-treated animals showed complex retinal alterations with improvements in some parameters while deterioration in others. Our results point towards the retinotoxicity of vardenafil, even without diabetes, which raises doubts about the retinal safety of long-term continuous vardenafil administration. This effect needs to be considered when approving PDE inhibitors for alternative indications.
    MeSH term(s) Vardenafil Dihydrochloride/pharmacology ; Vardenafil Dihydrochloride/toxicity ; Animals ; Rats ; Rats, Zucker ; Phosphodiesterase 5 Inhibitors/pharmacology ; Male ; Diabetes Mellitus, Experimental/drug therapy ; Diabetes Mellitus, Type 2/drug therapy ; Diabetic Retinopathy/drug therapy ; Diabetic Retinopathy/pathology ; Retina/drug effects ; Retina/pathology ; Ependymoglial Cells/drug effects ; Ependymoglial Cells/pathology ; Ependymoglial Cells/metabolism
    Language English
    Publishing date 2024-04-13
    Publishing country England
    Document type Journal Article
    ZDB-ID 80122-7
    ISSN 1096-0007 ; 0014-4835
    ISSN (online) 1096-0007
    ISSN 0014-4835
    DOI 10.1016/j.exer.2024.109890
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  3. Article ; Online: Immunocytochemical analysis of misplaced rhodopsin-positive cells in the developing rodent retina.

    Szabó, Klaudia / Szabó, Arnold / Enzsöly, Anna / Szél, Agoston / Lukáts, Akos

    Cell and tissue research

    2014  Volume 356, Issue 1, Page(s) 49–63

    Abstract: During the first postnatal weeks of the developing rodent retina, rhodopsin can be detected in a number of neuron-like cells in the inner retina. In the present study, we aim to characterize the morphology, number and staining characteristics of this ... ...

    Abstract During the first postnatal weeks of the developing rodent retina, rhodopsin can be detected in a number of neuron-like cells in the inner retina. In the present study, we aim to characterize the morphology, number and staining characteristics of this peculiar population. Misplaced rhodopsin-positive cells (MRCs) were analyzed on retinas of four rodent species, labeled with various rhodopsin-specific antibodies. To investigate their possible relation with non-photoreceptor cells, sections were double-stained against distinct retinal cell types and proteins of the phototransduction cascade. The possibility of synapse formation and apoptosis were also investigated. In all species studied, misplaced cells comprised a few percent of all rhodopsin-positive elements. This ratio declined from the end of the second week and MRCs disappeared nearly completely from the retina by P24. MRCs resembled resident neurons of the inner retina, while outer segment-like processes were seen only rarely. MRCs expressed no other photopigment types and showed no colocalization with any of the bipolar, horizontal, amacrine and ganglion cell markers used. While all MRCs colabeled for arrestin and recoverin, other proteins of the phototransduction cascade were only detectable in a minority of the population. Only a few MRCs were shown to form synaptic-like endings. Our results showed that, during development, some rhodopsin-expressing cells are displaced to the inner retinal layers. Although most MRCs lack morphological features of photoreceptors, they contain some but not all, elements of the phototransduction cascade, indicating that they are most probably misplaced rods that failed to complete differentiation and integrate into the photoreceptor mosaic.
    MeSH term(s) Amacrine Cells/cytology ; Amacrine Cells/metabolism ; Animals ; Apoptosis ; Cricetinae ; Ependymoglial Cells/cytology ; Ependymoglial Cells/metabolism ; Immunohistochemistry ; Light Signal Transduction ; Mice ; Mice, Inbred C57BL ; Microglia/cytology ; Microglia/metabolism ; Rats ; Rats, Sprague-Dawley ; Retina/cytology ; Retina/growth & development ; Retina/metabolism ; Retinal Cone Photoreceptor Cells/cytology ; Retinal Cone Photoreceptor Cells/metabolism ; Retinal Neurons/cytology ; Retinal Neurons/metabolism ; Rhodopsin/metabolism ; Rod Opsins/metabolism ; Synapses/metabolism
    Chemical Substances Rod Opsins ; melanopsin ; Rhodopsin (9009-81-8)
    Language English
    Publishing date 2014-04
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 125067-x
    ISSN 1432-0878 ; 0302-766X
    ISSN (online) 1432-0878
    ISSN 0302-766X
    DOI 10.1007/s00441-013-1788-2
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  4. Article: Immunocytochemical analysis of misplaced rhodopsin-positive cells in the developing rodent retina

    Szabó, Klaudia / Szabó, Arnold / Énzsöly, Anna / Szél, Ágoston / Lukáts, Ákos

    Cell and tissue research. 2014 Apr., v. 356, no. 1

    2014  

    Abstract: During the first postnatal weeks of the developing rodent retina, rhodopsin can be detected in a number of neuron-like cells in the inner retina. In the present study, we aim to characterize the morphology, number and staining characteristics of this ... ...

    Abstract During the first postnatal weeks of the developing rodent retina, rhodopsin can be detected in a number of neuron-like cells in the inner retina. In the present study, we aim to characterize the morphology, number and staining characteristics of this peculiar population. Misplaced rhodopsin-positive cells (MRCs) were analyzed on retinas of four rodent species, labeled with various rhodopsin-specific antibodies. To investigate their possible relation with non-photoreceptor cells, sections were double-stained against distinct retinal cell types and proteins of the phototransduction cascade. The possibility of synapse formation and apoptosis were also investigated. In all species studied, misplaced cells comprised a few percent of all rhodopsin-positive elements. This ratio declined from the end of the second week and MRCs disappeared nearly completely from the retina by P24. MRCs resembled resident neurons of the inner retina, while outer segment-like processes were seen only rarely. MRCs expressed no other photopigment types and showed no colocalization with any of the bipolar, horizontal, amacrine and ganglion cell markers used. While all MRCs colabeled for arrestin and recoverin, other proteins of the phototransduction cascade were only detectable in a minority of the population. Only a few MRCs were shown to form synaptic-like endings. Our results showed that, during development, some rhodopsin-expressing cells are displaced to the inner retinal layers. Although most MRCs lack morphological features of photoreceptors, they contain some but not all, elements of the phototransduction cascade, indicating that they are most probably misplaced rods that failed to complete differentiation and integrate into the photoreceptor mosaic.
    Keywords antibodies ; apoptosis ; ganglia ; neurons ; photoreceptors ; phototransduction ; retina ; rhodopsin ; rodents ; synapse
    Language English
    Dates of publication 2014-04
    Size p. 49-63.
    Publishing place Springer-Verlag
    Document type Article
    ZDB-ID 125067-x
    ISSN 1432-0878 ; 0302-766X
    ISSN (online) 1432-0878
    ISSN 0302-766X
    DOI 10.1007/s00441-013-1788-2
    Database NAL-Catalogue (AGRICOLA)

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  5. Article ; Online: Novel features of neurodegeneration in the inner retina of early diabetic rats.

    Énzsöly, Anna / Szabó, Arnold / Szabó, Klaudia / Szél, Ágoston / Németh, János / Lukáts, Ákos

    Histology and histopathology

    2015  Volume 30, Issue 8, Page(s) 971–985

    Abstract: The literature indicates that in diabetes retinal dysfunctions related to neural retinal alterations exist prior to clinically detectable vasculopathy. In a previous report, a detailed description about the alteration of the outer retina was given, where ...

    Abstract The literature indicates that in diabetes retinal dysfunctions related to neural retinal alterations exist prior to clinically detectable vasculopathy. In a previous report, a detailed description about the alteration of the outer retina was given, where diabetic degeneration preceded apoptotic loss of cells (Enzsöly et al., 2014). Here, we investigated the histopathology of the inner retina in early diabetes using the same specimens. We examined rat retinas with immunohistochemistry and Western blotting, 12 weeks after streptozotocin induction of diabetes. Glial reactivity was observed in all diabetic retinal specimens; however, it was not detectable all over the retina, but appeared in randomly arranged patches, with little or no glia activation in between. Similarly, immunoreactivity of parvalbumin (staining mostly AII amacrine cells) was also decreased only in some regions. We propose that these focal changes appear prior to affecting the whole retina and overt loss of cells. In contrast to these, most other markers used (calretinin, recoverin, tyrosin hydroxylase anti-Brn-3a and also calbindin in the optic part of the retina) did not show any major alterations in the intensity of immunoreactivity or in the number of stained elements. Interestingly, under diabetic conditions, the labeling pattern of PKC-α and calbindin in the ciliary retina showed a clear resemblance to the pattern described during development. This observation is in line with our previous study, reporting an increase in the number of dual cones, coexpressing two photopigments, which is another common feature with developing retinas. These data may indicate a previously uninvestigated regenerative capacity in diabetic retina.
    MeSH term(s) Amacrine Cells/metabolism ; Animals ; Apoptosis ; Blotting, Western ; Cell Count ; Diabetes Mellitus, Experimental/pathology ; Diabetic Retinopathy/pathology ; Image Processing, Computer-Assisted ; Immunohistochemistry ; Macrophage Activation ; Male ; Neurodegenerative Diseases/pathology ; Neuroglia/pathology ; Parvalbumins/metabolism ; Rats ; Rats, Wistar ; Retina/pathology ; Retinal Bipolar Cells/pathology ; Retinal Ganglion Cells/pathology
    Chemical Substances Parvalbumins
    Language English
    Publishing date 2015-08
    Publishing country Spain
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 83911-5
    ISSN 1699-5848 ; 0213-3911
    ISSN (online) 1699-5848
    ISSN 0213-3911
    DOI 10.14670/HH-11-602
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Is a neuronal chain between the pineal body and the retina in rats and hamsters? Transneural tracing studies.

    Csáki, Ágnes / Vígh, Béla / Boldogkői, Zsolt / Vereczki, Viktoria / Szél, Ágoston / Köves, Katalin

    Neuroscience letters

    2015  Volume 588, Page(s) 1–6

    Abstract: Neuronal chains between the retina and the pineal body were investigated. Transneuronal tracers, retrograde spreading pseudorabies virus (labeled with green fluorescent protein, memGreen-RV) and virus spreading in both ante- and retrograde directions ( ... ...

    Abstract Neuronal chains between the retina and the pineal body were investigated. Transneuronal tracers, retrograde spreading pseudorabies virus (labeled with green fluorescent protein, memGreen-RV) and virus spreading in both ante- and retrograde directions (labeled with red fluorescent protein, Ka-VHS-mCherry-A-RV) were injected into the right eye of vitreous body of intact or bilaterally sympathectomized Wistar male rats. Intact golden hamsters also received memGreen-RV into the eye and Ka-VHS-mCherry-A-RV into the pineal body. Four-five days later the animals were sacrificed. Frozen sections were prepared from the removed structures. In intact rats memGreen-RV resulted in green fluorescent labeling in the trigeminal and the superior cervical ganglia, the lateral horn of the spinal cord, the paraventricular and the suprachiasmatic nuclei, the perifornical region, the ventrolateral medulla, the locus ceruleus, and the raphe nuclei. In sympathectomized rats the labeling was missing from the brainstem but further existed in the hypothalamus. This observation indicates that the hypothalamic labeling is not mediated by the sympathetic system. One labeled neuron in the pineal body was only observed in 2/13 rats. It was independent from the sympathectomy. When the animals received Ka-VHS-mCherry-A-RV the distribution of the labeling was very similar to that of the intact group receiving retrograde virus. In golden hamsters the memGreen-RV labeled structures were seen in similar places as in rats, but virus labeled nerve cell bodies were always seen in the pineal body. Injection of Ka-VHS-mCherry-A-RV into the pineal body of hamsters resulted in labeling of the retina at both sides. It was concluded that the retinopetal neuronal chain in golden hamsters is always present but in rats it is stochastic.
    MeSH term(s) Animals ; Cricetinae ; Female ; Herpesvirus 1, Suid ; Male ; Mesocricetus ; Neurons/cytology ; Neurons/physiology ; Pineal Gland/cytology ; Pineal Gland/physiology ; Rats, Wistar ; Retina/cytology ; Retina/physiology ; Species Specificity ; Sympathectomy
    Language English
    Publishing date 2015-02-19
    Publishing country Ireland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 194929-9
    ISSN 1872-7972 ; 0304-3940
    ISSN (online) 1872-7972
    ISSN 0304-3940
    DOI 10.1016/j.neulet.2014.12.043
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  7. Article ; Online: Detailed Evaluation of Possible Ganglion Cell Loss in the Retina of Zucker Diabetic Fatty (ZDF) Rats.

    Hajdú, Rozina I / Laurik, Lenke K / Szabó, Klaudia / Dékány, Bulcsú / Almási, Zsuzsanna / Énzsöly, Anna / Szabó, Arnold / Radovits, Tamás / Mátyás, Csaba / Oláh, Attila / Szél, Ágoston / Somfai, Gábor M / Dávid, Csaba / Lukáts, Ákos

    Scientific reports

    2019  Volume 9, Issue 1, Page(s) 10463

    Abstract: A thinning of the inner retina is one of the earliest potential markers of neuroretinal damage in diabetic subjects. The histological background is uncertain; retinal ganglion cell (RGC) loss and changes in the structure or thickness of the inner ... ...

    Abstract A thinning of the inner retina is one of the earliest potential markers of neuroretinal damage in diabetic subjects. The histological background is uncertain; retinal ganglion cell (RGC) loss and changes in the structure or thickness of the inner plexiform layer (IPL) have been suspected. Studies conducted on animal models on RGC pathology gave contradictory results. Hereby we present RGC numbers, distribution patterns and IPL thickness from Zucker Diabetic Fatty (ZDF) rats. After labelling RGCs on retinal whole mounts, isodensity maps were constructed, RGC numbers and distribution patterns analysed using a custom-built algorithm, enabling point-by-point comparison. There was no change in staining characteristics of the antibodies and no significant difference in average RGC densities was found compared to controls. The distribution patterns were also comparable and no significant difference was found in IPL thickness and stratification or in the number of apoptotic cells in the ganglion cell layer (GCL). Our results provide a detailed evaluation of the inner retina and exclude major RGC loss in ZDF rats and suggest that other factors could serve as a potential explanation for inner retinal thinning in clinical studies. Our custom-built method could be adopted for the assessment of other animal or human retinas.
    MeSH term(s) Animals ; Apoptosis ; Blood Glucose/metabolism ; Body Weight ; Diabetes Mellitus, Experimental/physiopathology ; Male ; Optic Nerve/metabolism ; Optic Nerve/pathology ; Rats ; Rats, Zucker ; Retinal Ganglion Cells/metabolism ; Retinal Ganglion Cells/pathology
    Chemical Substances Blood Glucose
    Language English
    Publishing date 2019-07-18
    Publishing country England
    Document type Evaluation Study ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-019-46879-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Peripheral autonomic nerves of human pineal organ terminate on vessels, their supposed role in the periodic secretion of pineal melatonin.

    Manzano E Silva, Maria Joao / Singh, Royana / Haldar, Chandana / Vigh, Béla / Szél, Ágoston

    APMIS : acta pathologica, microbiologica, et immunologica Scandinavica

    2012  Volume 120, Issue 8, Page(s) 628–634

    Abstract: Nonvisual pineal and retinal photoreceptors are synchronizing circadian and circannual periodicity to the environmental light periods in the function of various organs. Melatonin of the pineal organ is secreted at night and represents an important factor ...

    Abstract Nonvisual pineal and retinal photoreceptors are synchronizing circadian and circannual periodicity to the environmental light periods in the function of various organs. Melatonin of the pineal organ is secreted at night and represents an important factor of this periodic regulation. Night illumination suppressing melatonin secretion may result in pathological events like breast and colorectal cancer. Experimental works demonstrated the role of autonomic nerves in the pineal melatonin secretion. It was supposed that mammalian pineals have lost their photoreceptor capacity that is present in submammalians, and sympathetic fibers would mediate light information from the retina to regulate melatonin secretion. Retinal afferentation may reach the organ by central nerve fibers via the pineal habenulae as well. In our earlier works we have found that the pineal organ developing from lobular evaginations of the epithalamus differs from peripheral endocrine glands and is composed of a retina-like central nervous tissue that is comprised of cone-like pinealocytes, secondary pineal neurons and glial cells. Their autonomic nerves in submammalians as well as in mammalian animals do not terminate on pineal cells, rather, they run in the meningeal septa among pineal lobules and form vasomotor nerve endings. Concerning the adult human pineal there are no detailed fine structural data about the termination of autonomic fibers, therefore, in the present work we investigated the ultrastructure of the human pineal peripheral autonomic nerve fibers. It was found, that similarly to other parts of the brain, autonomic nerves do not enter the human pineal nervous tissue itself but separated by glial limiting membranes take their course in the meningeal septa of the organ and terminate on vessels by vasomotor endings. We suppose that these autonomic vasomotor nerves serve the regulation of the pineal blood supply according to the circadian and circannual changes of the metabolic activity of the organ and support by this effect the secretion of pineal neurohormones including melatonin.
    MeSH term(s) Autonomic Nervous System/physiology ; Circadian Clocks/physiology ; Humans ; Light ; Melatonin/metabolism ; Melatonin/secretion ; Nerve Endings/physiology ; Nerve Fibers/physiology ; Neuroglia/metabolism ; Neuroglia/physiology ; Peripheral Nervous System/physiology ; Photoreceptor Cells/physiology ; Photoreceptor Cells, Vertebrate/physiology ; Pineal Gland/innervation ; Pineal Gland/metabolism ; Pineal Gland/secretion ; Retina/physiology ; Vasomotor System/metabolism ; Vasomotor System/physiology
    Chemical Substances Melatonin (JL5DK93RCL)
    Language English
    Publishing date 2012-08
    Publishing country Denmark
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 93340-5
    ISSN 1600-0463 ; 0903-4641
    ISSN (online) 1600-0463
    ISSN 0903-4641
    DOI 10.1111/j.1600-0463.2011.02867.x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Pathologic alterations of the outer retina in streptozotocin-induced diabetes.

    Énzsöly, Anna / Szabó, Arnold / Kántor, Orsolya / Dávid, Csaba / Szalay, Péter / Szabó, Klaudia / Szél, Ágoston / Németh, János / Lukáts, Ákos

    Investigative ophthalmology & visual science

    2014  Volume 55, Issue 6, Page(s) 3686–3699

    Abstract: Purpose: Neurodegeneration as an early event of diabetic retinopathy preceding clinically detectable vascular alterations is a widely proven issue today. While there is evidence for the impairment of color vision and contrast sensitivity in early ... ...

    Abstract Purpose: Neurodegeneration as an early event of diabetic retinopathy preceding clinically detectable vascular alterations is a widely proven issue today. While there is evidence for the impairment of color vision and contrast sensitivity in early diabetes, suggesting deteriorated photoreceptor function, the underlying neuropathology of these functional alterations is still unknown. The aim of the present study was to investigate the effects of early diabetes on the outer retinal cells.
    Methods: The retinal pigment epithelium, photopigment expression, and density and morphology of photoreceptors were studied using immunocytochemistry in streptozotocin-induced diabetes in two rat strains. The fine structure of photoreceptors and pigment epithelium was also investigated with transmission electron microscopy.
    Results: Here we found that retinal thickness was unchanged in diabetic animals and that no significant increase in the number of apoptotic cells was present. Although the density of cones expressing middle (M)- and shortwave (S)-sensitive opsins was similar in diabetic and control retinas, we detected remarkable morphologic signs of degeneration in the outer segments of diabetic rods, most M-cones, and some S-cones. A decrease in thickness and RPE65 protein immunoreactivity of the pigment epithelium were evident. Furthermore, an increased number of dual cones, coexpressing both M- and S-opsins, was detected at the peripheral retina of diabetic rats.
    Conclusions: Degenerative changes of photoreceptors and pigment epithelium shown here prior to apoptotic loss of photoreceptors may contribute to functional alterations reported in diabetic human patients and different animal models, thus may serve as a potential model for testing the efficacy of neuroprotective agents in diabetes.
    MeSH term(s) Animals ; Apoptosis ; Cell Count ; Diabetes Mellitus, Experimental/complications ; Diabetes Mellitus, Experimental/metabolism ; Diabetes Mellitus, Experimental/pathology ; Diabetic Retinopathy/etiology ; Diabetic Retinopathy/metabolism ; Diabetic Retinopathy/pathology ; Disease Progression ; Immunohistochemistry ; In Situ Nick-End Labeling ; Lectins/metabolism ; Male ; Microscopy, Electron, Transmission ; Rats ; Rats, Sprague-Dawley ; Rats, Wistar ; Retinal Photoreceptor Cell Outer Segment/metabolism ; Retinal Photoreceptor Cell Outer Segment/ultrastructure ; Retinal Pigment Epithelium/metabolism ; Retinal Pigment Epithelium/ultrastructure
    Chemical Substances Lectins
    Language English
    Publishing date 2014-05-20
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 391794-0
    ISSN 1552-5783 ; 0146-0404
    ISSN (online) 1552-5783
    ISSN 0146-0404
    DOI 10.1167/iovs.13-13562
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  10. Article ; Online: Histological Evaluation of Diabetic Neurodegeneration in the Retina of Zucker Diabetic Fatty (ZDF) Rats.

    Szabó, Klaudia / Énzsöly, Anna / Dékány, Bulcsú / Szabó, Arnold / Hajdú, Rozina I / Radovits, Tamás / Mátyás, Csaba / Oláh, Attila / Laurik, Lenke K / Somfai, Gábor M / Merkely, Béla / Szél, Ágoston / Lukáts, Ákos

    Scientific reports

    2017  Volume 7, Issue 1, Page(s) 8891

    Abstract: In diabetes, retinal dysfunctions exist prior to clinically detectable vasculopathy, however the pathology behind these functional deficits is still not fully established. Previously, our group published a detailed study on the retinal histopathology of ... ...

    Abstract In diabetes, retinal dysfunctions exist prior to clinically detectable vasculopathy, however the pathology behind these functional deficits is still not fully established. Previously, our group published a detailed study on the retinal histopathology of type 1 diabetic (T1D) rat model, where specific alterations were detected. Although the majority of human diabetic patients have type 2 diabetes (T2D), similar studies on T2D models are practically absent. To fill this gap, we examined Zucker Diabetic Fatty (ZDF) rats - a model for T2D - by immunohistochemistry at the age of 32 weeks. Glial reactivity was observed in all diabetic specimens, accompanied by an increase in the number of microglia cells. Prominent outer segment degeneration was detectable with changes in cone opsin expression pattern, without a decrease in the number of labelled elements. The immunoreactivity of AII amacrine cells was markedly decreased and changes were detectable in the number and staining of some other amacrine cell subtypes, while most other cells examined did not show any major alterations. Overall, the retinal histology of ZDF rats shows a surprising similarity to T1D rats indicating that despite the different evolution of the disease, the neuroretinal cells affected are the same in both subtypes of diabetes.
    MeSH term(s) Amacrine Cells/metabolism ; Animals ; Apoptosis ; Blood Glucose ; Body Weight ; Diabetes Mellitus, Experimental ; Diabetes Mellitus, Type 2/complications ; Diabetes Mellitus, Type 2/metabolism ; Diabetes Mellitus, Type 2/pathology ; Diabetic Nephropathies/metabolism ; Diabetic Nephropathies/pathology ; Diabetic Retinopathy/metabolism ; Diabetic Retinopathy/pathology ; Disease Models, Animal ; Male ; Mice, Transgenic ; Microglia/metabolism ; Microglia/pathology ; Photoreceptor Cells/metabolism ; Photoreceptor Cells/pathology ; Rats ; Rats, Zucker ; Retinal Pigment Epithelium/metabolism
    Chemical Substances Blood Glucose
    Language English
    Publishing date 2017-08-21
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-017-09068-6
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