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Inflamed In Vitro Retina: Cytotoxic Neuroinflammation and Galectin-3 Expression.

BACKGROUNDDisease progression in retinal neurodegeneration is strongly correlated to immune cell activation, which may have either a neuroprotective or neurotoxic effect. Increased knowledge about the immune response profile and retinal neurodegeneration may lead to candidate targets for treatments.... Full description

Journal Title: PloS one 2016, Vol.11(9), p.e0161723
Main Author: Bauer, Patrik Maximilian
Other Authors: Zalis, Marina Castro , Abdshill, Hodan , Deierborg, Tomas , Johansson, Fredrik , Englund-Johansson, Ulrica
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 1932-6203 ; DOI: 1932-6203 ; DOI: 10.1371/journal.pone.0161723
Link: http://search.proquest.com/docview/1819122692/?pq-origsite=primo
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title: Inflamed In Vitro Retina: Cytotoxic Neuroinflammation and Galectin-3 Expression.
format: Article
creator:
  • Bauer, Patrik Maximilian
  • Zalis, Marina Castro
  • Abdshill, Hodan
  • Deierborg, Tomas
  • Johansson, Fredrik
  • Englund-Johansson, Ulrica
subjects:
  • Animals–Drug Effects
  • Apoptosis–Metabolism
  • Calcium-Binding Proteins–Metabolism
  • Ectodysplasins–Genetics
  • Galectin 3–Metabolism
  • Gene Expression Regulation–Drug Effects
  • Glial Fibrillary Acidic Protein–Metabolism
  • In Vitro Techniques–Chemically Induced
  • Inflammation–Metabolism
  • Interleukin-2–Metabolism
  • Interleukin-6–Metabolism
  • Ki-67 Antigen–Toxicity
  • Lipopolysaccharides–Metabolism
  • Mice–Cytology
  • Microfilament Proteins–Drug Effects
  • Microglia–Metabolism
  • Neurons–Drug Effects
  • Retina–Cytology
  • Tumor Necrosis Factor-Alpha–Drug Effects
  • Tumor Necrosis Factor-Alpha–Metabolism
  • Tumor Necrosis Factor-Alpha–Metabolism
  • Aif1 Protein, Mouse
  • Calcium-Binding Proteins
  • Ectodysplasins
  • Eda Protein, Mouse
  • Galectin 3
  • Glial Fibrillary Acidic Protein
  • Interleukin-2
  • Interleukin-6
  • Ki-67 Antigen
  • Lipopolysaccharides
  • Microfilament Proteins
  • Tumor Necrosis Factor-Alpha
  • Glial Fibrillary Astrocytic Protein, Mouse
ispartof: PloS one, 2016, Vol.11(9), p.e0161723
description: BACKGROUNDDisease progression in retinal neurodegeneration is strongly correlated to immune cell activation, which may have either a neuroprotective or neurotoxic effect. Increased knowledge about the immune response profile and retinal neurodegeneration may lead to candidate targets for treatments. Therefore, we have used the explanted retina as a model to explore the immune response and expression of the immune modulator galectin-3 (Gal-3), induced by the cultivation per se and after additional immune stimulation with lipopolysaccharide (LPS), and how this correlates with retinal neurotoxicity. METHODSPost-natal mouse retinas were cultured in a defined medium. One group was stimulated with LPS (100 ng/ml, 24 h). Retinal architecture, apoptotic cell death, and micro- and macroglial activity were studied at the time of cultivation (0 days in vitro (DIV)) and at 3, 4 and 7 DIV using morphological staining, biochemical- and immunohistochemical techniques. RESULTSOur results show that sustained activation of macro- and microglia, characterized by no detectable cytokine release and limited expression of Gal-3, is not further inducing apoptosis additional to the axotomy-induced apoptosis in innermost nuclear layer. An elevated immune response was detected after LPS stimulation, as demonstrated primarily by release of immune mediators (i.e. interleukin 2 (IL-2), IL-6, KC/GRO (also known as CLCX1) and tumour necrosis factor-α (TNF-α)), increased numbers of microglia displaying morphologies of late activation stages as well as Gal-3 expression. This was accompanied with increased apoptosis in the two additional nuclear layers, and damage to retinal gross architecture. CONCLUSIONWe demonstrate that an immune response characterized by sustained and increased release of cytokines, along with an increase in Gal-3 expression, is accompanied by significant increased neurotoxicity in the explanted retina. Further investigations using the current setting may lead to increased understanding on the mechanisms involved in neuronal loss in retinal neurodegenerations.
language: eng
source:
identifier: E-ISSN: 1932-6203 ; DOI: 1932-6203 ; DOI: 10.1371/journal.pone.0161723
fulltext: fulltext
issn:
  • 19326203
  • 1932-6203
url: Link


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titleInflamed In Vitro Retina: Cytotoxic Neuroinflammation and Galectin-3 Expression.
creatorBauer, Patrik Maximilian ; Zalis, Marina Castro ; Abdshill, Hodan ; Deierborg, Tomas ; Johansson, Fredrik ; Englund-Johansson, Ulrica
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subjectAnimals–Drug Effects ; Apoptosis–Metabolism ; Calcium-Binding Proteins–Metabolism ; Ectodysplasins–Genetics ; Galectin 3–Metabolism ; Gene Expression Regulation–Drug Effects ; Glial Fibrillary Acidic Protein–Metabolism ; In Vitro Techniques–Chemically Induced ; Inflammation–Metabolism ; Interleukin-2–Metabolism ; Interleukin-6–Metabolism ; Ki-67 Antigen–Toxicity ; Lipopolysaccharides–Metabolism ; Mice–Cytology ; Microfilament Proteins–Drug Effects ; Microglia–Metabolism ; Neurons–Drug Effects ; Retina–Cytology ; Tumor Necrosis Factor-Alpha–Drug Effects ; Tumor Necrosis Factor-Alpha–Metabolism ; Tumor Necrosis Factor-Alpha–Metabolism ; Aif1 Protein, Mouse ; Calcium-Binding Proteins ; Ectodysplasins ; Eda Protein, Mouse ; Galectin 3 ; Glial Fibrillary Acidic Protein ; Interleukin-2 ; Interleukin-6 ; Ki-67 Antigen ; Lipopolysaccharides ; Microfilament Proteins ; Tumor Necrosis Factor-Alpha ; Glial Fibrillary Astrocytic Protein, Mouse
descriptionBACKGROUNDDisease progression in retinal neurodegeneration is strongly correlated to immune cell activation, which may have either a neuroprotective or neurotoxic effect. Increased knowledge about the immune response profile and retinal neurodegeneration may lead to candidate targets for treatments. Therefore, we have used the explanted retina as a model to explore the immune response and expression of the immune modulator galectin-3 (Gal-3), induced by the cultivation per se and after additional immune stimulation with lipopolysaccharide (LPS), and how this correlates with retinal neurotoxicity. METHODSPost-natal mouse retinas were cultured in a defined medium. One group was stimulated with LPS (100 ng/ml, 24 h). Retinal architecture, apoptotic cell death, and micro- and macroglial activity were studied at the time of cultivation (0 days in vitro (DIV)) and at 3, 4 and 7 DIV using morphological staining, biochemical- and immunohistochemical techniques. RESULTSOur results show that sustained activation of macro- and microglia, characterized by no detectable cytokine release and limited expression of Gal-3, is not further inducing apoptosis additional to the axotomy-induced apoptosis in innermost nuclear layer. An elevated immune response was detected after LPS stimulation, as demonstrated primarily by release of immune mediators (i.e. interleukin 2 (IL-2), IL-6, KC/GRO (also known as CLCX1) and tumour necrosis factor-α (TNF-α)), increased numbers of microglia displaying morphologies of late activation stages as well as Gal-3 expression. This was accompanied with increased apoptosis in the two additional nuclear layers, and damage to retinal gross architecture. CONCLUSIONWe demonstrate that an immune response characterized by sustained and increased release of cytokines, along with an increase in Gal-3 expression, is accompanied by significant increased neurotoxicity in the explanted retina. Further investigations using the current setting may lead to increased understanding on the mechanisms involved in neuronal loss in retinal neurodegenerations.
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titleInflamed In Vitro Retina: Cytotoxic Neuroinflammation and Galectin-3 Expression.
descriptionBACKGROUNDDisease progression in retinal neurodegeneration is strongly correlated to immune cell activation, which may have either a neuroprotective or neurotoxic effect. Increased knowledge about the immune response profile and retinal neurodegeneration may lead to candidate targets for treatments. Therefore, we have used the explanted retina as a model to explore the immune response and expression of the immune modulator galectin-3 (Gal-3), induced by the cultivation per se and after additional immune stimulation with lipopolysaccharide (LPS), and how this correlates with retinal neurotoxicity. METHODSPost-natal mouse retinas were cultured in a defined medium. One group was stimulated with LPS (100 ng/ml, 24 h). Retinal architecture, apoptotic cell death, and micro- and macroglial activity were studied at the time of cultivation (0 days in vitro (DIV)) and at 3, 4 and 7 DIV using morphological staining, biochemical- and immunohistochemical techniques. RESULTSOur results show that sustained activation of macro- and microglia, characterized by no detectable cytokine release and limited expression of Gal-3, is not further inducing apoptosis additional to the axotomy-induced apoptosis in innermost nuclear layer. An elevated immune response was detected after LPS stimulation, as demonstrated primarily by release of immune mediators (i.e. interleukin 2 (IL-2), IL-6, KC/GRO (also known as CLCX1) and tumour necrosis factor-α (TNF-α)), increased numbers of microglia displaying morphologies of late activation stages as well as Gal-3 expression. This was accompanied with increased apoptosis in the two additional nuclear layers, and damage to retinal gross architecture. CONCLUSIONWe demonstrate that an immune response characterized by sustained and increased release of cytokines, along with an increase in Gal-3 expression, is accompanied by significant increased neurotoxicity in the explanted retina. Further investigations using the current setting may lead to increased understanding on the mechanisms involved in neuronal loss in retinal neurodegenerations.
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6Glial Fibrillary Acidic Protein–Metabolism
7In Vitro Techniques–Chemically Induced
8Inflammation–Metabolism
9Interleukin-2–Metabolism
10Interleukin-6–Metabolism
11Ki-67 Antigen–Toxicity
12Lipopolysaccharides–Metabolism
13Mice–Cytology
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titleInflamed In Vitro Retina: Cytotoxic Neuroinflammation and Galectin-3 Expression.
authorBauer, Patrik Maximilian ; Zalis, Marina Castro ; Abdshill, Hodan ; Deierborg, Tomas ; Johansson, Fredrik ; Englund-Johansson, Ulrica
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6Glial Fibrillary Acidic Protein–Metabolism
7In Vitro Techniques–Chemically Induced
8Inflammation–Metabolism
9Interleukin-2–Metabolism
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13Mice–Cytology
14Microfilament Proteins–Drug Effects
15Microglia–Metabolism
16Neurons–Drug Effects
17Retina–Cytology
18Tumor Necrosis Factor-Alpha–Drug Effects
19Tumor Necrosis Factor-Alpha–Metabolism
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22Ectodysplasins
23Eda Protein, Mouse
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25Glial Fibrillary Acidic Protein
26Interleukin-2
27Interleukin-6
28Ki-67 Antigen
29Lipopolysaccharides
30Microfilament Proteins
31Tumor Necrosis Factor-Alpha
32Glial Fibrillary Astrocytic Protein, Mouse
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abstractBACKGROUNDDisease progression in retinal neurodegeneration is strongly correlated to immune cell activation, which may have either a neuroprotective or neurotoxic effect. Increased knowledge about the immune response profile and retinal neurodegeneration may lead to candidate targets for treatments. Therefore, we have used the explanted retina as a model to explore the immune response and expression of the immune modulator galectin-3 (Gal-3), induced by the cultivation per se and after additional immune stimulation with lipopolysaccharide (LPS), and how this correlates with retinal neurotoxicity. METHODSPost-natal mouse retinas were cultured in a defined medium. One group was stimulated with LPS (100 ng/ml, 24 h). Retinal architecture, apoptotic cell death, and micro- and macroglial activity were studied at the time of cultivation (0 days in vitro (DIV)) and at 3, 4 and 7 DIV using morphological staining, biochemical- and immunohistochemical techniques. RESULTSOur results show that sustained activation of macro- and microglia, characterized by no detectable cytokine release and limited expression of Gal-3, is not further inducing apoptosis additional to the axotomy-induced apoptosis in innermost nuclear layer. An elevated immune response was detected after LPS stimulation, as demonstrated primarily by release of immune mediators (i.e. interleukin 2 (IL-2), IL-6, KC/GRO (also known as CLCX1) and tumour necrosis factor-α (TNF-α)), increased numbers of microglia displaying morphologies of late activation stages as well as Gal-3 expression. This was accompanied with increased apoptosis in the two additional nuclear layers, and damage to retinal gross architecture. CONCLUSIONWe demonstrate that an immune response characterized by sustained and increased release of cytokines, along with an increase in Gal-3 expression, is accompanied by significant increased neurotoxicity in the explanted retina. Further investigations using the current setting may lead to increased understanding on the mechanisms involved in neuronal loss in retinal neurodegenerations.
doi10.1371/journal.pone.0161723
urlhttp://search.proquest.com/docview/1819122692/
isbn9789177534754
date2016-01-01