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[PMID]:28456012
[Au] Autor:Alizadeh A; Dyck SM; Kataria H; Shahriary GM; Nguyen DH; Santhosh KT; Karimi-Abdolrezaee S
[Ad] Endereço:Regenerative Medicine Program, Department of Physiology and Pathophysiology, Spinal Cord Research Centre, University of Manitoba, Winnipeg, Manitoba, R3E 0J9, Canada.
[Ti] Título:Neuregulin-1 positively modulates glial response and improves neurological recovery following traumatic spinal cord injury.
[So] Source:Glia;65(7):1152-1175, 2017 Jul.
[Is] ISSN:1098-1136
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Spinal cord injury (SCI) results in glial activation and neuroinflammation, which play pivotal roles in the secondary injury mechanisms with both pro- and antiregeneration effects. Presently, little is known about the endogenous molecular mechanisms that regulate glial functions in the injured spinal cord. We previously reported that the expression of neuregulin-1 (Nrg-1) is acutely and chronically declined following traumatic SCI. Here, we investigated the potential ramifications of Nrg-1 dysregulation on glial and immune cell reactivity following SCI. Using complementary in vitro approaches and a clinically-relevant model of severe compressive SCI in rats, we demonstrate that immediate delivery of Nrg-1 (500 ng/day) after injury enhances a neuroprotective phenotype in inflammatory cells associated with increased interleukin-10 and arginase-1 expression. We also found a decrease in proinflammatory factors including IL-1ß, TNF-α, matrix metalloproteinases (MMP-2 and 9) and nitric oxide after injury. In addition, Nrg-1 modulates astrogliosis and scar formation by reducing inhibitory chondroitin sulfate proteoglycans after SCI. Mechanistically, Nrg-1 effects on activated glia are mediated through ErbB2 tyrosine phosphorylation in an ErbB2/3 heterodimer complex. Furthermore, Nrg-1 exerts its effects through downregulation of MyD88, a downstream adaptor of Toll-like receptors, and increased phosphorylation of Erk1/2 and STAT3. Nrg-1 treatment with the therapeutic dosage of 1.5 µg/day significantly improves tissue preservation and functional recovery following SCI. Our findings for the first time provide novel insights into the role and mechanisms of Nrg-1 in acute SCI and suggest a positive immunomodulatory role for Nrg-1 that can harness the beneficial properties of activated glia and inflammatory cells in recovery following SCI.
[Mh] Termos MeSH primário: Doenças do Sistema Nervoso/tratamento farmacológico
Doenças do Sistema Nervoso/etiologia
Neuregulina-1/uso terapêutico
Neuroglia/fisiologia
Recuperação de Função Fisiológica/fisiologia
Traumatismos da Medula Espinal/complicações
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Arginase/metabolismo
Células Cultivadas
Meios de Cultivo Condicionados/farmacologia
Modelos Animais de Doenças
Feminino
Regulação da Expressão Gênica/efeitos dos fármacos
Regulação da Expressão Gênica/fisiologia
Proteína Glial Fibrilar Ácida/metabolismo
Interleucina-10/metabolismo
Lipopolissacarídeos/toxicidade
Locomoção/efeitos dos fármacos
Camundongos
Camundongos Endogâmicos C57BL
Neuregulina-1/metabolismo
Neuregulina-1/farmacologia
Neuroglia/efeitos dos fármacos
Ratos
Recuperação de Função Fisiológica/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
Traumatismos da Medula Espinal/patologia
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Culture Media, Conditioned); 0 (Glial Fibrillary Acidic Protein); 0 (Lipopolysaccharides); 0 (Neuregulin-1); 130068-27-8 (Interleukin-10); EC 3.5.3.1 (Arginase); EC 3.5.3.1 (arginase I, rat)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE
[do] DOI:10.1002/glia.23150


  2 / 14493 MEDLINE  
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[PMID]:27778377
[Au] Autor:Kyyriäinen J; Ekolle Ndode-Ekane X; Pitkänen A
[Ad] Endereço:Department of Neurobiology, A. I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, FI-70211, Finland.
[Ti] Título:Dynamics of PDGFRß expression in different cell types after brain injury.
[So] Source:Glia;65(2):322-341, 2017 02.
[Is] ISSN:1098-1136
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Platelet-derived growth factor receptor ß (PDGFRß) is upregulated after brain injury and its depletion results in the blood-brain barrier (BBB) damage. We investigated the time-window and localization of PDGFRß expression in mice with intrahippocampal kainic acid-induced status epilepticus (SE) and in rats with lateral fluid-percussion-induced traumatic brain injury (TBI). Tissue immunohistochemistry was evaluated at several time-points after SE and TBI. The distribution of PDGFRß was analyzed, and its cell type-specific expression was verified with double/triple-labeling of astrocytes (GFAP), NG2 cells, and endothelial cells (RECA-1). In normal mouse hippocampus, we found evenly distributed PDGFRß+ parenchymal cells. In double-labeling, all NG2+ and 40%-60% GFAP+ cells were PDGFRß+. After SE, PDGFRß+ cells clustered in the ipsilateral hilus (178% of that in controls at fourth day, 225% at seventh day, P < 0.05) and in CA3 (201% at seventh day, P < 0.05), but the total number of PDGFRß+ cells was not altered. As in controls, PDGFRß-immunoreactivity was detected in parenchymal NG2+ and GFAP+ cells. We also observed PDGFRß+ structural pericytes, detached reactive pericytes, and endothelial cells. After TBI, PDGFRß+ cells clustered in the perilesional cortex and thalamus, particularly during the first post-injury week. PDGFRß immunopositivity was observed in NG2+ and GFAP+ cells, structural pericytes, detached reactive pericytes, and endothelial cells. In some animals, PDGFRß vascular staining was observed around the cortical glial scar for up to 3 months. Our data revealed an acute accumulation of PDGFRß+ BBB-related cells in degenerating brain areas, which can be long lasting, suggesting an active role for PDGFRß-signaling in blood vessel and post-injury tissue recovery. GLIA 2017;65:322-341.
[Mh] Termos MeSH primário: Astrócitos/classificação
Astrócitos/metabolismo
Lesões Encefálicas/patologia
Células Endoteliais/metabolismo
Molécula-1 de Adesão Celular Endotelial de Plaquetas/metabolismo
Receptor alfa de Fator de Crescimento Derivado de Plaquetas/metabolismo
[Mh] Termos MeSH secundário: Animais
Antígenos/metabolismo
Modelos Animais de Doenças
Proteína Glial Fibrilar Ácida/metabolismo
Proteínas de Fluorescência Verde/genética
Proteínas de Fluorescência Verde/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Pericitos/metabolismo
Pericitos/patologia
Proteoglicanas/metabolismo
Ratos
Ratos Sprague-Dawley
Receptor alfa de Fator de Crescimento Derivado de Plaquetas/genética
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens); 0 (Glial Fibrillary Acidic Protein); 0 (Platelet Endothelial Cell Adhesion Molecule-1); 0 (Proteoglycans); 0 (chondroitin sulfate proteoglycan 4); 147336-22-9 (Green Fluorescent Proteins); EC 2.7.10.1 (Receptor, Platelet-Derived Growth Factor alpha)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.1002/glia.23094


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[PMID]:29351334
[Au] Autor:Chang W; Lajko M; Fawzi AA
[Ad] Endereço:Department of Ophthalmology, Northwestern University, Feinberg School of Medicine, Chicago, IL, United States of America.
[Ti] Título:Endothelin-1 is associated with fibrosis in proliferative diabetic retinopathy membranes.
[So] Source:PLoS One;13(1):e0191285, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: To characterize the relationship between endothelin-1 and fibrosis in epiretinal membranes in proliferative diabetic retinopathy and explore the role of endothelial-mesenchymal transition in these membranes. METHODS: Membranes were obtained from eyes undergoing pars plana vitrectomy for complicated proliferative diabetic retinopathy or idiopathic epiretinal membrane. Through standard immunohistochemical techniques, we labeled membranes to explore the distribution of endothelin-1 and endothelin receptor B, comparing proliferative diabetic retinopathy and idiopathic epiretinal membranes. In addition, membranes were also labeled with markers for fibroblasts, endothelial, and glial cells and studied with confocal laser scanning microscopy. The intensity of endothelin-1 labeling was quantified using standard image analysis software. RESULTS: Fourteen membranes were included in the analysis, nine from eyes with proliferative diabetic retinopathy and five idiopathic membranes. Flatmount diabetic membranes showed co-localization of endothelin-1 with S100A4 and CD31. Immunohistochemistry and quantitative analysis of cross-sectional membranes showed significantly higher endothelin-1 labeling in proliferative diabetic retinopathy membranes compared to idiopathic membranes (p<0.05). Diabetic membranes showed more elements staining positive for S100A4 compared to idiopathic membranes. CONCLUSION: Epiretinal membrane formation in proliferative diabetic retinopathy involves higher tissue levels of endothelin-1 and fibroblastic activity. Furthermore, endothelin-1, endothelial and fibroblastic staining appear to be correlated, suggestive of endothelial-to-mesenchymal transition in proliferative diabetic retinopathy.
[Mh] Termos MeSH primário: Retinopatia Diabética/metabolismo
Retinopatia Diabética/patologia
Endotelina-1/metabolismo
[Mh] Termos MeSH secundário: Adulto
Proliferação Celular
Feminino
Fibrose
Proteína Glial Fibrilar Ácida/metabolismo
Seres Humanos
Masculino
Membranas/patologia
Meia-Idade
Molécula-1 de Adesão Celular Endotelial de Plaquetas/metabolismo
Retina/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Endothelin-1); 0 (Glial Fibrillary Acidic Protein); 0 (Platelet Endothelial Cell Adhesion Molecule-1)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180120
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191285


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[PMID]:28746897
[Au] Autor:Song W; Cressatti M; Zukor H; Liberman A; Galindez C; Schipper HM
[Ad] Endereço:Bloomfield Centre for Research in Aging, Lady Davis Institute, Jewish General Hospital, Montreal, Quebec, Canada.
[Ti] Título:Parkinsonian features in aging GFAP.HMOX1 transgenic mice overexpressing human HO-1 in the astroglial compartment.
[So] Source:Neurobiol Aging;58:163-179, 2017 Oct.
[Is] ISSN:1558-1497
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Epigenetic influences mediating brain iron deposition, oxidative mitochondrial injury, and macroautophagy in Parkinson disease and related conditions remain enigmatic. Here, we show that selective overexpression of the stress protein, heme oxygenase-1 (HO-1) in astrocytes of GFAP.HMOX1 transgenic mice between 8.5 and 19 months of age results in nigrostriatal hypodopaminergia associated with locomotor incoordination and stereotypy; downregulation of tyrosine hydroxylase, DAT, LMX1B, Nurr1, Pitx3 and DJ-1 mRNA and/or protein; overproduction of α-synuclein and ubiquitin; oxidative stress; basal ganglia siderosis; mitochondrial damage/mitophagy; and augmented GABAergic systems (increased GABA, GAD67 and reelin). The neurophenotype of these GFAP.HMOX1 mice is highly consistent with parkinsonism and differs dramatically from the schizophrenia-like features previously documented in younger GFAP.HMOX1 mice. Common stressors may elicit either early-onset developmental (schizophrenia) or later-life degenerative (PD) brain disorders depending on whether the glial HO-1 response is engaged prior to or following the maturation of dopaminergic circuitry. Curtailment of glial HO-1 transduction at strategic points of the life course may confer neuroprotection in human degenerative and developmental central nervous system disorders.
[Mh] Termos MeSH primário: Astrócitos/enzimologia
Expressão Gênica/genética
Proteína Glial Fibrilar Ácida/genética
Heme Oxigenase-1/genética
Heme Oxigenase-1/metabolismo
Proteínas de Membrana/genética
Doença de Parkinson/genética
[Mh] Termos MeSH secundário: Animais
Autofagia
Células Cultivadas
Dopamina/metabolismo
Seres Humanos
Camundongos Transgênicos
Mitocôndrias/patologia
Estresse Oxidativo
Doença de Parkinson/metabolismo
Doença de Parkinson/patologia
alfa-Sinucleína/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glial Fibrillary Acidic Protein); 0 (Membrane Proteins); 0 (alpha-Synuclein); EC 1.14.14.18 (HMOX1 protein, human); EC 1.14.14.18 (Heme Oxygenase-1); EC 1.14.14.18 (Hmox1 protein, mouse); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE


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[PMID]:29025656
[Au] Autor:Xia B; Lv Y
[Ad] Endereço:Key Laboratory of Biorheological Science and Technology (Chongqing University), Ministry of Education, Bioengineering College, Chongqing University, Chongqing 400044, PR China; Mechanobiology and Regenerative Medicine Laboratory, Bioengineering College, Chongqing University, Chongqing 400044, PR China.
[Ti] Título:Dual-delivery of VEGF and NGF by emulsion electrospun nanofibrous scaffold for peripheral nerve regeneration.
[So] Source:Mater Sci Eng C Mater Biol Appl;82:253-264, 2018 Jan 01.
[Is] ISSN:1873-0191
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Controlled delivery of multiple therapeutic agents can be considered an effective approach in nerve injury due to its multifunction. In this study, recombinant human vascular endothelial growth factor (VEGF) and recombinant human nerve growth factor (NGF) were loaded on the surface and in the core of emulsion electrospun poly (l-lactic acid) (PLLA) nanofibrous scaffold, respectively. The in vitro studies showed that VEGF and NGF had a sequential release pattern in which most of the VEFG was released in the first few days but the NGF could be continuously released for >1month. The dual-delivery scaffold could enhance the neural differentiation of induced pluripotent stem cells-derived neural crest stem cells (iPSCs-NCSCs) in vitro. Furthermore, this scaffold was applied to a critical sized defect in rat sciatic nerve model. Footprint analysis, electrophysiological tests, and histological analysis revealed that a significant improvement of neovascularization as well as nerve healing after 3months post-operation could be achieved by dual-delivery of VEGF and NGF. Taken together, the present study indicated that VEGF and NGF in emulsion electrospun nanofibrous scaffold had a synergistic effect on regeneration of vascularized nerve tissue.
[Mh] Termos MeSH primário: Emulsões/química
Nanofibras/química
Fator de Crescimento Neural/química
Nervo Isquiático/fisiologia
Tecidos Suporte/química
Fator A de Crescimento do Endotélio Vascular/química
[Mh] Termos MeSH secundário: Animais
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Células Cultivadas
Feminino
Expressão Gênica/efeitos dos fármacos
Proteína Glial Fibrilar Ácida/genética
Proteína Glial Fibrilar Ácida/metabolismo
Células-Tronco Pluripotentes Induzidas/citologia
Células-Tronco Pluripotentes Induzidas/metabolismo
Proteínas Associadas aos Microtúbulos/genética
Proteínas Associadas aos Microtúbulos/metabolismo
Fator de Crescimento Neural/farmacologia
Regeneração Nervosa/efeitos dos fármacos
Células-Tronco Neurais/citologia
Células-Tronco Neurais/metabolismo
Poliésteres/química
Ratos
Ratos Sprague-Dawley
Recuperação de Função Fisiológica
Nervo Isquiático/patologia
Fator A de Crescimento do Endotélio Vascular/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Emulsions); 0 (Glial Fibrillary Acidic Protein); 0 (Microtubule-Associated Proteins); 0 (Polyesters); 0 (Vascular Endothelial Growth Factor A); 459TN2L5F5 (poly(lactide)); 9061-61-4 (Nerve Growth Factor)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180205
[Lr] Data última revisão:
180205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171014
[St] Status:MEDLINE


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[PMID]:29261743
[Au] Autor:Bharani KL; Derex R; Granholm AC; Ledreux A
[Ad] Endereço:Department of Neurosciences, Medical University of South Carolina, BSB, Charleston, SC, United States of America.
[Ti] Título:A noradrenergic lesion aggravates the effects of systemic inflammation on the hippocampus of aged rats.
[So] Source:PLoS One;12(12):e0189821, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neuroinflammation is potentiated by early degeneration of the locus coeruleus noradrenergic pathway (LC-NE) commonly seen in aging-related neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. In animal models, lipopolysaccharide (LPS) induces strong peripheral immune responses that can cause cognitive changes secondary to neuroinflammation. The influence of the peripheral immune response on cognition might be exacerbated by LC-NE degeneration, but this has not been well characterized previously. In this study, we investigated how systemic inflammation affects neuroinflammation and cognition in aged rats that have had either normal or damaged LC-NE transmitter systems. Rats were first exposed to the selective noradrenergic (NE) neurotoxin N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP4) to induce degeneration of central NE pathways. Two weeks later, the rats received a low dose of LPS. This resulted in 3 treatment groups (Control, LPS-, and DSP4+LPS-treated rats) studied at 4 hours (short-term subgroup) and 7 days (long-term subgroup) following the LPS injection. DSP4+LPS-treated rats exhibited increased serum levels of several pro-inflammatory cytokines, increased astroglial and microglial activation in the hippocampus, and poorer performance in the novel object recognition task (NORT) compared to controls and LPS-treated rats. Additionally, serum and brain tissue levels of brain-derived neurotrophic factor (BDNF) were modulated over time in the DSP4+LPS group compared to the other two groups. Specifically, DSP4+LPS-treated rats in the short-term subgroup had lower hippocampal BDNF levels (~25%) than controls and LPS-treated rats, which negatively correlated with hippocampal astrogliosis and positively correlated with hippocampal IL-1ß levels. Serum and hippocampal BDNF levels in the DSP4+LPS-treated rats in the long-term subgroup returned to levels similar to the control group. These results show that systemic inflammation in LC-NE-lesioned aged rats promotes an exacerbated systemic and central inflammatory response compared to LC-NE-intact rats and alters BDNF levels, indicating the important role of this neurotransmitter system in response to neuroinflammation.
[Mh] Termos MeSH primário: Envelhecimento/patologia
Hipocampo/patologia
Inflamação/patologia
Norepinefrina/metabolismo
[Mh] Termos MeSH secundário: Análise de Variância
Animais
Astrócitos/patologia
Benzilaminas
Fator Neurotrófico Derivado do Encéfalo/sangue
Fator Neurotrófico Derivado do Encéfalo/metabolismo
Proteínas de Ligação ao Cálcio/metabolismo
Quimiocinas/sangue
Discriminação (Psicologia)
Imunofluorescência
Proteína Glial Fibrilar Ácida/metabolismo
Hipocampo/fisiopatologia
Inflamação/sangue
Interleucina-1beta/metabolismo
Lipopolissacarídeos
Locomoção
Masculino
Proteínas dos Microfilamentos/metabolismo
Microglia/patologia
Degeneração Neural/patologia
Ratos Endogâmicos F344
Análise e Desempenho de Tarefas
Tirosina 3-Mono-Oxigenase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aif1 protein, rat); 0 (Benzylamines); 0 (Brain-Derived Neurotrophic Factor); 0 (Calcium-Binding Proteins); 0 (Chemokines); 0 (Glial Fibrillary Acidic Protein); 0 (Interleukin-1beta); 0 (Lipopolysaccharides); 0 (Microfilament Proteins); EC 1.14.16.2 (Tyrosine 3-Monooxygenase); PQ1P7JP5C1 (DSP 4); X4W3ENH1CV (Norepinephrine)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189821


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[PMID]:28465658
[Au] Autor:Godisela KK; Reddy SS; Kumar CU; Saravanan N; Reddy PY; Jablonski MM; Ayyagari R; Reddy GB
[Ad] Endereço:National Institute of Nutrition, Hyderabad, India.
[Ti] Título:Impact of obesity with impaired glucose tolerance on retinal degeneration in a rat model of metabolic syndrome.
[So] Source:Mol Vis;23:263-274, 2017.
[Is] ISSN:1090-0535
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Metabolic syndrome (MetS) is associated with several degenerative diseases, including retinal degeneration. Previously, we reported on progressive retinal degeneration in a spontaneous obese rat (WNIN/Ob) model. In this study, we investigated the additional effect of impaired glucose tolerance (IGT), an essential component of MetS, on retinal degeneration using the WNIN/GR-Ob rat model. METHODS: The retinal morphology and ultrastructure of WNIN/GR-Ob and age-matched littermate lean rats were studied by microscopy and immunohistochemistry. The retinal transcriptome of WNIN/GR-Ob was compared with the respective lean controls and with the WNIN/Ob model using microarray analysis. Expression of selected retinal marker genes was studied via real-time PCR. RESULTS: Progressive loss of photoreceptor cells was observed in WNIN/GR-Ob rats with an onset as early as 3 months. Similarly, thinning of the inner nuclear layer was observed from 6 months in these rats. Immunohistochemical analysis showed decreased levels of rhodopsin and postsynaptic density protein-95 (PSD-95) proteins and increased levels of glial fibrillary acidic protein (GFAP), vascular endothelial growth factor (VEGF), and calretinin in WNIN/GR-Ob rats compared with the age-matched lean controls, further supporting cellular stress/damage and retinal degeneration. The retinal transcriptome analysis indicated altered expression profiles in both the WNIN/GR-Ob and WNIN/Ob rat models compared to their respective lean controls; these pathways are associated with activation of pathways like cellular oxidative stress response, inflammation, apoptosis, and phototransduction, although the changes were more prominent in WNIN/GR-Ob than in WNIN/Ob animals. CONCLUSIONS: WNIN/GR-Ob rats with added glucose intolerance developed retinal degeneration similar to the parent line WNIN/Ob. The severity of retinal degeneration was greater in WNIN/GR-Ob rats compared to WNIN/Ob, suggesting a possible role for IGT in this model. Hence, the WNIN/GR-Ob model could be a valuable tool for investigating the impact of MetS on retinal degeneration pathology.
[Mh] Termos MeSH primário: Modelos Animais de Doenças
Intolerância à Glucose/complicações
Síndrome Metabólica/etiologia
Obesidade/complicações
Degeneração Retiniana/etiologia
[Mh] Termos MeSH secundário: Animais
Calbindina 2/metabolismo
Proteína 4 Homóloga a Disks-Large/metabolismo
Proteína Glial Fibrilar Ácida/metabolismo
Intolerância à Glucose/metabolismo
Intolerância à Glucose/fisiopatologia
Masculino
Síndrome Metabólica/metabolismo
Síndrome Metabólica/fisiopatologia
Obesidade/metabolismo
Obesidade/fisiopatologia
Células Fotorreceptoras de Vertebrados/patologia
Ratos
Ratos Wistar
Reação em Cadeia da Polimerase em Tempo Real
Degeneração Retiniana/metabolismo
Degeneração Retiniana/fisiopatologia
Rodopsina/metabolismo
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calb2 protein, rat); 0 (Calbindin 2); 0 (Disks Large Homolog 4 Protein); 0 (Dlg4 protein, rat); 0 (Glial Fibrillary Acidic Protein); 0 (Vascular Endothelial Growth Factor A); 0 (glial fibrillary acid protein, rat); 0 (vascular endothelial growth factor A, rat); 9009-81-8 (Rhodopsin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


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[PMID]:29176876
[Au] Autor:Stifter J; Ulbrich F; Goebel U; Böhringer D; Lagrèze WA; Biermann J
[Ad] Endereço:Eye Center, Medical Center-University of Freiburg, Killianstrasse 5, Freiburg, Germany.
[Ti] Título:Neuroprotection and neuroregeneration of retinal ganglion cells after intravitreal carbon monoxide release.
[So] Source:PLoS One;12(11):e0188444, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Retinal ischemia induces apoptosis leading to neurodegeneration and vision impairment. Carbon monoxide (CO) in gaseous form showed cell-protective and anti-inflammatory effects after retinal ischemia-reperfusion-injury (IRI). These effects were also demonstrated for the intravenously administered CO-releasing molecule (CORM) ALF-186. This article summarizes the results of intravitreally released CO to assess its suitability as a neuroprotective and neuroregenerative agent. METHODS: Water-soluble CORM ALF-186 (25 µg), PBS, or inactivated ALF (iALF) (all 5 µl) were intravitreally applied into the left eyes of rats directly after retinal IRI for 1 h. Their right eyes remained unaffected and were used for comparison. Retinal tissue was harvested 24 h after intervention to analyze mRNA or protein expression of Caspase-3, pERK1/2, p38, HSP70/90, NF-kappaB, AIF-1 (allograft inflammatory factor), TNF-α, and GAP-43. Densities of fluorogold-prelabeled retinal ganglion cells (RGC) were examined in flat-mounted retinae seven days after IRI and were expressed as mean/mm2. The ability of RGC to regenerate their axon was evaluated two and seven days after IRI using retinal explants in laminin-1-coated cultures. Immunohistochemistry was used to analyze the different cell types growing out of the retinal explants. RESULTS: Compared to the RGC-density in the contralateral right eyes (2804±214 RGC/mm2; data are mean±SD), IRI+PBS injection resulted in a remarkable loss of RGC (1554±159 RGC/mm2), p<0.001. Intravitreally injected ALF-186 immediately after IRI provided RGC protection and reduced the extent of RGC-damage (IRI+PBS 1554±159 vs. IRI+ALF 2179±286, p<0.001). ALF-186 increased the IRI-mediated phosphorylation of MAP-kinase p38. Anti-apoptotic and anti-inflammatory effects were detectable as Caspase-3, NF-kappaB, TNF-α, and AIF-1 expression were significantly reduced after IRI+ALF in comparison to IRI+PBS or IRI+iALF. Gap-43 expression was significantly increased after IRI+ALF. iALF showed effects similar to PBS. The intrinsic regenerative potential of RGC-axons was induced to nearly identical levels after IRI and ALF or iALF-treatment under growth-permissive conditions, although RGC viability differed significantly in both groups. Intravitreal CO further increased the IRI-induced migration of GFAP-positive cells out of retinal explants and their transdifferentiation, which was detected by re-expression of beta-III tubulin and nestin. CONCLUSION: Intravitreal CORM ALF-186 protected RGC after IRI and stimulated their axons to regenerate in vitro. ALF conveyed anti-apoptotic, anti-inflammatory, and growth-associated signaling after IRI. CO's role in neuroregeneration and its effect on retinal glial cells needs further investigation.
[Mh] Termos MeSH primário: Monóxido de Carbono/metabolismo
Regeneração Nervosa
Neuroproteção
Células Ganglionares da Retina/metabolismo
[Mh] Termos MeSH secundário: Animais
Axônios/efeitos dos fármacos
Axônios/metabolismo
Proteínas de Ligação ao Cálcio/genética
Proteínas de Ligação ao Cálcio/metabolismo
Caspase 3/genética
Caspase 3/metabolismo
Movimento Celular/efeitos dos fármacos
Células Cultivadas
Complexos de Coordenação/administração & dosagem
Complexos de Coordenação/farmacologia
Complexos de Coordenação/uso terapêutico
Feminino
Proteína GAP-43/genética
Proteína GAP-43/metabolismo
Proteína Glial Fibrilar Ácida/metabolismo
Proteínas de Choque Térmico HSP70/metabolismo
Proteínas de Choque Térmico HSP90/metabolismo
Injeções Intravítreas
Masculino
Proteínas dos Microfilamentos/genética
Proteínas dos Microfilamentos/metabolismo
Proteínas Quinases Ativadas por Mitógeno/metabolismo
NF-kappa B/genética
NF-kappa B/metabolismo
Regeneração Nervosa/efeitos dos fármacos
Neuroglia/efeitos dos fármacos
Neuroglia/metabolismo
Neuroproteção/efeitos dos fármacos
Fármacos Neuroprotetores/farmacologia
Fármacos Neuroprotetores/uso terapêutico
Fosforilação/efeitos dos fármacos
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Ratos Sprague-Dawley
Traumatismo por Reperfusão/tratamento farmacológico
Traumatismo por Reperfusão/genética
Traumatismo por Reperfusão/patologia
Células Ganglionares da Retina/efeitos dos fármacos
Células Ganglionares da Retina/patologia
Tubulina (Proteína)/metabolismo
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aif1 protein, rat); 0 (Calcium-Binding Proteins); 0 (Coordination Complexes); 0 (GAP-43 Protein); 0 (Glial Fibrillary Acidic Protein); 0 (HSP70 Heat-Shock Proteins); 0 (HSP90 Heat-Shock Proteins); 0 (Microfilament Proteins); 0 (NF-kappa B); 0 (Neuroprotective Agents); 0 (RNA, Messenger); 0 (Tubb3 protein, rat); 0 (Tubulin); 0 (Tumor Necrosis Factor-alpha); 0 (triscarbonyl(histidinato)molybdate(III)); 7U1EE4V452 (Carbon Monoxide); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); EC 3.4.22.- (Caspase 3)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171219
[Lr] Data última revisão:
171219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188444


  9 / 14493 MEDLINE  
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[PMID]:29050386
[Au] Autor:Tong J; Rathitharan G; Meyer JH; Furukawa Y; Ang LC; Boileau I; Guttman M; Hornykiewicz O; Kish SJ
[Ad] Endereço:Preclinical Imaging Unit, Research Imaging Centre, Centre for Addiction and Mental Health, Toronto, Ontario, Canada.
[Ti] Título:Brain monoamine oxidase B and A in human parkinsonian dopamine deficiency disorders.
[So] Source:Brain;140(9):2460-2474, 2017 Sep 01.
[Is] ISSN:1460-2156
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:See Jellinger (doi:10.1093/awx190) for a scientific commentary on this article. The enzyme monoamine oxidases (B and A subtypes, encoded by MAOB and MAOA, respectively) are drug targets in the treatment of Parkinson's disease. Inhibitors of MAOB are used clinically in Parkinson's disease for symptomatic purposes whereas the potential disease-modifying effect of monoamine oxidase inhibitors is debated. As astroglial cells express high levels of MAOB, the enzyme has been proposed as a brain imaging marker of astrogliosis, a cellular process possibly involved in Parkinson's disease pathogenesis as elevation of MAOB in astrocytes might be harmful. Since brain monoamine oxidase status in Parkinson's disease is uncertain, our objective was to measure, by quantitative immunoblotting in autopsied brain homogenates, protein levels of both monoamine oxidases in three different degenerative parkinsonian disorders: Parkinson's disease (n = 11), multiple system atrophy (n = 11), and progressive supranuclear palsy (n = 16) and in matched controls (n = 16). We hypothesized that if MAOB is 'substantially' localized to astroglial cells, MAOB levels should be generally associated with standard astroglial protein measures (e.g. glial fibrillary acidic protein). MAOB levels were increased in degenerating putamen (+83%) and substantia nigra (+10%, non-significant) in multiple system atrophy; in caudate (+26%), putamen (+27%), frontal cortex (+31%) and substantia nigra (+23%) of progressive supranuclear palsy; and in frontal cortex (+33%), but not in substantia nigra of Parkinson's disease, a region we previously reported no increase in astrocyte protein markers. Although the magnitude of MAOB increase was less than those of standard astrocytic markers, significant positive correlations were observed amongst the astrocyte proteins and MAOB. Despite suggestions that MAOA (versus MAOB) is primarily responsible for metabolism of dopamine in dopamine neurons, there was no loss of the enzyme in the parkinsonian substantia nigra; instead, increased nigral levels of a MAOA fragment and 'turnover' of the enzyme were observed in the conditions. Our findings provide support that MAOB might serve as a biochemical imaging marker, albeit not entirely specific, for astrocyte activation in human brain. The observation that MAOB protein concentration is generally increased in degenerating brain areas in multiple system atrophy (especially putamen) and in progressive supranuclear palsy, but not in the nigra in Parkinson's disease, also distinguishes astrocyte behaviour in Parkinson's disease from that in the two 'Parkinson-plus' conditions. The question remains whether suppression of either MAOB in astrocytes or MAOA in dopamine neurons might influence progression of the parkinsonian disorders.
[Mh] Termos MeSH primário: Encéfalo/enzimologia
Dopamina/deficiência
Monoaminoxidase/metabolismo
Atrofia de Múltiplos Sistemas/metabolismo
Doença de Parkinson/metabolismo
Paralisia Supranuclear Progressiva/metabolismo
[Mh] Termos MeSH secundário: Adolescente
Adulto
Estudos de Casos e Controles
Núcleo Caudado/metabolismo
Feminino
Lobo Frontal/metabolismo
Proteína Glial Fibrilar Ácida/metabolismo
Seres Humanos
Isoenzimas/metabolismo
Masculino
Meia-Idade
Atrofia de Múltiplos Sistemas/patologia
Degeneração Neural/patologia
Doença de Parkinson/patologia
Fragmentos de Peptídeos/metabolismo
Fosfopiruvato Hidratase/metabolismo
Putamen/metabolismo
Substância Negra/metabolismo
Paralisia Supranuclear Progressiva/patologia
Tubulina (Proteína)/metabolismo
Adulto Jovem
alfa-Sinucleína/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glial Fibrillary Acidic Protein); 0 (Isoenzymes); 0 (Peptide Fragments); 0 (Tubulin); 0 (alpha-Synuclein); EC 1.4.3.4 (Monoamine Oxidase); EC 4.2.1.11 (Phosphopyruvate Hydratase); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171021
[St] Status:MEDLINE
[do] DOI:10.1093/brain/awx172


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[PMID]:29049715
[Au] Autor:Obana A; Sasano H; Okazaki S; Otsuki Y; Seto T; Gohto Y
[Ad] Endereço:Department of Ophthalmology, Seirei Hamamatsu General Hospital, Naka-ku, Hamamatsu City, Shizuoka, Japan.
[Ti] Título:Evidence of Carotenoid in Surgically Removed Lamellar Hole-Associated Epiretinal Proliferation.
[So] Source:Invest Ophthalmol Vis Sci;58(12):5157-5163, 2017 Oct 01.
[Is] ISSN:1552-5783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose: To determine the constituents and origin of the yellow pigment in surgically removed lamellar hole-associated epiretinal proliferation (LHEP) in patients with lamellar macular hole (LMH). Methods: This prospective case series comprised nine eyes with LMH in patients aged 41 to 83 years. The presence of LHEP was confirmed by preoperative optical coherence tomography; the distribution of macular pigment was observed by two-wavelength fundus autofluorescence technique before and after surgery. The subjects underwent a 25-gauge vitrectomy, and the surgically removed epiretinal membranous tissue was fixed with formalin. The specimens were examined using resonance Raman microscopy, and paraffin sections were stained with antiglial fibrillary acidic protein. Results: Seven cases presented with LHEP, and the presence of yellow pigment was confirmed using an operating microscope. Carotenoid-specific Raman signals with three major Raman peaks could be identified in the specimens with LHEP. These specimens were positive for glial fibrillary acidic protein staining. Using the fundus autofluorescence technique, a central defect in the distribution of the macular pigment was noted in the exact area of the lamellar hole. This type of defect was no longer visible after surgical repair of the lamellar hole. Conclusions: The constituents of the yellow pigment in the removed LHEP were carotenoids that typically originate from the macular xanthophyll pigments at the fovea. Since LHEP is reported to be composed of Müller cells, we hypothesize that xanthophyll carotenoids at the fovea are contained in the Müller cells.
[Mh] Termos MeSH primário: Membrana Epirretiniana/metabolismo
Pigmento Macular/metabolismo
Perfurações Retinianas/metabolismo
Xantofilas/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Biomarcadores/metabolismo
Membrana Epirretiniana/diagnóstico
Membrana Epirretiniana/cirurgia
Feminino
Fundo de Olho
Proteína Glial Fibrilar Ácida/metabolismo
Seres Humanos
Masculino
Meia-Idade
Estudos Prospectivos
Perfurações Retinianas/diagnóstico
Perfurações Retinianas/cirurgia
Análise Espectral Raman
Tomografia de Coerência Óptica
Acuidade Visual
Vitrectomia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Glial Fibrillary Acidic Protein); 0 (Macular Pigment); 0 (Xanthophylls)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171027
[Lr] Data última revisão:
171027
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171020
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.17-22347



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