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  1 / 2428 MEDLINE  
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[PMID]:28986598
[Au] Autor:Liu H; Anders F; Thanos S; Mann C; Liu A; Grus FH; Pfeiffer N; Prokosch-Willing V
[Ad] Endereço:Department of Ophthalmology, University Medical Centre, Johannes Gutenberg University Mainz, Germany.
[Ti] Título:Hydrogen Sulfide Protects Retinal Ganglion Cells Against Glaucomatous Injury In Vitro and In Vivo.
[So] Source:Invest Ophthalmol Vis Sci;58(12):5129-5141, 2017 Oct 01.
[Is] ISSN:1552-5783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose: Hydrogen sulfide (H2S) is recognized as a novel third signaling molecule and gaseous neurotransmitter. Recently, cell protective properties within the central nervous and cardiovascular system have been proposed. Our purpose was to analyze the expression and neuroprotective effects of H2S in experimental models of glaucoma. Methods: Elevated IOP was induced in Sprague-Dawley rats by means of episcleral vein cauterization. After 7 weeks, animals were killed and the retina was analyzed with label-free mass spectrometry. In vitro, retinal explants were exposed to elevated hydrostatic pressure or oxidative stress (H2O2), with and without addition of a slow-releasing H2S donor Morpholin-4-ium-methoxyphenyl-morpholino-phosphinodithioate (GYY4137). In vivo, GYY4137 was injected intravitreally in animals with acute ischemic injury or optic nerve crush. Brn3a+ retinal ganglion cells (RGCs) were counted in retinal flat mounts and compared. Optical coherence tomography (OCT) was performed to examine the vessels. Comparisons were made by t-test and ANOVA (P < 0.05). Results: IOP elevation caused significant RGC loss (P < 0.001); 3-mercaptosulfurtransferase, an H2S producing enzyme, showed a 3-fold upregulation within the retina after IOP elevation. GYY4137 protected RGCs against elevated pressure and oxidative stress in vitro depending on the concentration used (P < 0.005). In vivo, intravitreal administration of GYY4137 preserved RGCs from acute ischemic injury and optic nerve crush (P < 0.0001). Retinal vessel diameters enlarged after intravitreal GYY4137 injection (P < 0.0001). Conclusions: H2S is specifically regulated in experimental glaucoma. By scavenging reactive oxygen species and dilating retinal vessels, H2S may protect RGCs from pressure and oxidative stress-induced RGC loss in vitro and in vivo. Therefore, H2S might be a novel neuroprotectant in glaucoma.
[Mh] Termos MeSH primário: Modelos Animais de Doenças
Glaucoma/prevenção & controle
Sulfeto de Hidrogênio/farmacologia
Fármacos Neuroprotetores/farmacologia
Traumatismos do Nervo Óptico/prevenção & controle
Células Ganglionares da Retina/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Feminino
Peróxido de Hidrogênio/toxicidade
Pressão Hidrostática
Pressão Intraocular/efeitos dos fármacos
Morfolinas/farmacologia
Compressão Nervosa
Compostos Organotiofosforados/farmacologia
Estresse Oxidativo/efeitos dos fármacos
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GYY 4137); 0 (Morpholines); 0 (Neuroprotective Agents); 0 (Organothiophosphorus Compounds); BBX060AN9V (Hydrogen Peroxide); YY9FVM7NSN (Hydrogen Sulfide)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171008
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.17-22200


  2 / 2428 MEDLINE  
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[PMID]:28973334
[Au] Autor:Oku H; Morishita S; Horie T; Kida T; Mimura M; Kojima S; Ikeda T
[Ad] Endereço:Department of Ophthalmology, Osaka Medical College, Osaka, Japan.
[Ti] Título:P7C3 Suppresses Neuroinflammation and Protects Retinal Ganglion Cells of Rats from Optic Nerve Crush.
[So] Source:Invest Ophthalmol Vis Sci;58(11):4877-4888, 2017 Sep 01.
[Is] ISSN:1552-5783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose: To determine whether P7C3-A20 can inhibit the phosphorylation of the mammalian target of rapamycin (mTOR), depress neuroinflammation, and protect retinal ganglion cells (RGCs) of rats from optic nerve crush (ONC). Methods: The left optic nerve was crushed, and 5.0 mg/kg/d of P7C3-A20, 1.0 mg/kg/d of rapamycin, or their vehicle was injected intraperitoneally for 3 consecutive days beginning 1 day before the ONC. The protective effects on the RGCs were determined by immunohistochemical staining for Tuj-1. The level of phosphorylated mTOR was determined by immunoblotting. The neuroinflammation in the optic nerve was determined by changes in the expression of CD68, TNF-α, MCP-1, and iNOS. Results: The density of Tuj-1-stained cells in the control was 2010 ± 81.5/mm2 and 1842 ± 80.4/mm2 on days 7 and 14 after the sham operation. These levels were lower at 995 ± 122/mm2 and 450 ± 52.4/mm2 on days 7 and 14 after the ONC, respectively. Rapamycin and P7C3-A20 preserved the density at significantly higher levels on both days (P < 0.05, Scheffe test). The level of phosphorylated mTOR increased by 1.56-fold above the control level on day 7. Rapamycin and P7C3 significantly lowered the level of phosphorylated mTOR to 0.89-fold and 0.67-fold of the control, respectively. There was an accumulation of CD68+ cells that were immunoreactive to TNF-α at the crush site. The expression of MCP-1 and iNOS was increased chiefly in the astrocytes around the lesion. These inflammatory events were suppressed by both rapamycin and P7C3. Conclusions: P7C3-A20 can inhibit mTOR phosphorylation in the crushed optic nerve, which may suppress neuroinflammation and preserve the RGCs.
[Mh] Termos MeSH primário: Anti-Inflamatórios/uso terapêutico
Carbazóis/farmacologia
Fármacos Neuroprotetores/farmacologia
Traumatismos do Nervo Óptico/tratamento farmacológico
Nervo Óptico/patologia
Células Ganglionares da Retina/efeitos dos fármacos
Sirolimo/farmacologia
Serina-Treonina Quinases TOR/metabolismo
[Mh] Termos MeSH secundário: Animais
Biomarcadores/metabolismo
Modelos Animais de Doenças
Masculino
Compressão Nervosa
Traumatismos do Nervo Óptico/metabolismo
Traumatismos do Nervo Óptico/patologia
Fosforilação/efeitos dos fármacos
Ratos
Ratos Wistar
Células Ganglionares da Retina/metabolismo
Células Ganglionares da Retina/patologia
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Biomarkers); 0 (Carbazoles); 0 (Neuroprotective Agents); 0 (P7C3 compound); 0 (Tumor Necrosis Factor-alpha); EC 2.7.1.1 (MTOR protein, human); EC 2.7.1.1 (TOR Serine-Threonine Kinases); W36ZG6FT64 (Sirolimus)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171004
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.17-22179


  3 / 2428 MEDLINE  
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[PMID]:28912156
[Au] Autor:Lindborg JA; Mack M; Zigmond RE
[Ad] Endereço:Department of Neurosciences, Case Western Reserve University, Cleveland, Ohio 44106-4975, and.
[Ti] Título:Neutrophils Are Critical for Myelin Removal in a Peripheral Nerve Injury Model of Wallerian Degeneration.
[So] Source:J Neurosci;37(43):10258-10277, 2017 Oct 25.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Wallerian degeneration (WD) is considered an essential preparatory stage to the process of axonal regeneration. In the peripheral nervous system, infiltrating monocyte-derived macrophages, which use the chemokine receptor CCR2 to gain entry to injured tissues from the bloodstream, are purportedly necessary for efficient WD. However, our laboratory has previously reported that myelin clearance in the injured sciatic nerve proceeds unhindered in the mouse model. Here, we extensively characterize WD in male mice and identify a compensatory mechanism of WD that is facilitated primarily by neutrophils. In response to the loss of CCR2, injured sciatic nerves demonstrate prolonged expression of neutrophil chemokines, a concomitant extended increase in the accumulation of neutrophils in the nerve, and elevated phagocytosis by neutrophils. Neutrophil depletion substantially inhibits myelin clearance after nerve injury in both male WT and mice, highlighting a novel role for these cells in peripheral nerve degeneration that spans genotypes. The accepted view in the basic and clinical neurosciences is that the clearance of axonal and myelin debris after a nerve injury is directed primarily by inflammatory CCR2 macrophages. However, we demonstrate that this clearance is nearly identical in WT and mice, and that neutrophils replace CCR2 macrophages as the primary phagocytic cell. We find that neutrophils play a major role in myelin clearance not only in mice but also in WT mice, highlighting their necessity during nerve degeneration in the peripheral nervous system. These degeneration studies may propel improvements in nerve regeneration and draw critical parallels to mechanisms of nerve degeneration and regeneration in the CNS and in the context of peripheral neuropathies.
[Mh] Termos MeSH primário: Modelos Animais de Doenças
Bainha de Mielina/metabolismo
Neutrófilos/metabolismo
Neuropatia Ciática/metabolismo
Degeneração Walleriana/metabolismo
[Mh] Termos MeSH secundário: Animais
Feminino
Masculino
Camundongos
Camundongos da Linhagem 129
Camundongos Endogâmicos C57BL
Camundongos Knockout
Bainha de Mielina/patologia
Compressão Nervosa/métodos
Neutrófilos/patologia
Traumatismos dos Nervos Periféricos/metabolismo
Traumatismos dos Nervos Periféricos/patologia
Fagocitose/fisiologia
Distribuição Aleatória
Neuropatia Ciática/patologia
Degeneração Walleriana/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171115
[Lr] Data última revisão:
171115
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170916
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.2085-17.2017


  4 / 2428 MEDLINE  
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[PMID]:28652727
[Au] Autor:Song J; Li X; Li Y; Che J; Li X; Zhao X; Chen Y; Zheng X; Yuan W
[Ad] Endereço:Department of Orthopedics, Shanghai Jiao Tong University Affiliated Sixth People's Hospital.
[Ti] Título:Biodegradable and biocompatible cationic polymer delivering microRNA-221/222 promotes nerve regeneration after sciatic nerve crush.
[So] Source:Int J Nanomedicine;12:4195-4208, 2017.
[Is] ISSN:1178-2013
[Cp] País de publicação:New Zealand
[La] Idioma:eng
[Ab] Resumo:MicroRNA (miRNA) has great potential to treat a wide range of illnesses by regulating the expression of eukaryotic genes. Biomaterials with high transfection efficiency and low toxicity are needed to deliver miRNA to target cells. In this study, a biodegradable and biocompatible cationic polymer (PDAPEI) was synthetized from low molecular weight polyethyleneimine (PEI1.8kDa) cross-linked with 2,6-pyridinedicarboxaldehyde. PDAPEI showed a lower cytotoxicity and higher transfection efficiency than PEI25kDa in transfecting miR-221/222 into rat Schwann cells (SCs). The upregulation of miR-221/222 in SCs promoted the expression of nerve growth factor and myelin basic protein in vitro. The mouse sciatic nerve crush injury model was used to evaluate the effectiveness of PDAPEI/miR-221/222 complexes for nerve regeneration in vivo. The results of electrophysiological tests, functional assessments, and histological and immunohistochemistry analyses demonstrated that PDAPEI/miR-221/222 complexes significantly promoted nerve regeneration after sciatic nerve crush, specifically enhancing remyelination. All these results show that the use of PDAPEI to deliver miR-221/222 may provide a safe therapeutic means of treating nerve crush injury and may help to overcome the barrier of biomaterial toxicity and low efficiency often encountered during medical intervention.
[Mh] Termos MeSH primário: MicroRNAs/administração & dosagem
Regeneração Nervosa/genética
Polímeros/química
Nervo Isquiático/cirurgia
[Mh] Termos MeSH secundário: Animais
Materiais Biocompatíveis
Cátions
Modelos Animais de Doenças
Masculino
Camundongos
MicroRNAs/genética
Proteína Básica da Mielina/metabolismo
Nanopartículas/administração & dosagem
Nanopartículas/química
Compressão Nervosa
Fator de Crescimento Neural/metabolismo
Regeneração Nervosa/efeitos dos fármacos
Regeneração Nervosa/fisiologia
Polímeros/administração & dosagem
Ratos
Ratos Sprague-Dawley
Células de Schwann/metabolismo
Nervo Isquiático/lesões
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biocompatible Materials); 0 (Cations); 0 (MicroRNAs); 0 (Myelin Basic Protein); 0 (Polymers); 9061-61-4 (Nerve Growth Factor)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170628
[St] Status:MEDLINE
[do] DOI:10.2147/IJN.S132190


  5 / 2428 MEDLINE  
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[PMID]:28603016
[Au] Autor:Fan N; Silverman SM; Liu Y; Wang X; Kim BJ; Tang L; Clark AF; Liu X; Pang IH
[Ad] Endereço:Shenzhen Eye Hospital, Shenzhen Key Laboratory of Ophthalmology, Jinan University, Shenzhen, China; North Texas Eye Research Institute, University of North Texas Health Science Center, Fort Worth, TX, USA; Department of Pharmaceutical Sciences, University of North Texas Health Science Center, Fort W
[Ti] Título:Rapid repeatable in vivo detection of retinal reactive oxygen species.
[So] Source:Exp Eye Res;161:71-81, 2017 Aug.
[Is] ISSN:1096-0007
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Oxidative injuries, such as those related to reactive oxygen species (ROS), have been implicated in various retinal and optic nerve disorders. Many ROS detection methods have been developed. Although widely utilized, many of these methods are useful only in post mortem tissues, or require relatively expensive equipment, or involve intraocular injection. In the present study, we demonstrated and characterized a chemiluminescent probe L-012 as a noninvasive, in vivo ROS detection agent in the mouse retina. Using optic nerve crush (ONC) and retinal ischemia/reperfusion (I/R) as injury models, we show that L-012 produced intensive luminescent signals specifically in the injured eyes. Histological examination showed that L-012 administration was safe to the retina. Additionally, compounds that reduce tissue superoxide levels, apocynin and TEMPOL, decreased injury-induced L-012 chemiluminescence. The decrease in L-012 signals correlated with their protective effects against retinal I/R-induced morphological and functional changes in the retina. Together, these data demonstrate the feasibility of a fast, simple, reproducible, and non-invasive detection method to monitor in vivo ROS in the retina. Furthermore, the results also show that reduction of ROS is a potential therapeutic approach for protection from these retinal injuries.
[Mh] Termos MeSH primário: Traumatismos do Nervo Óptico/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Traumatismo por Reperfusão/metabolismo
Neurônios Retinianos/metabolismo
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Eletrorretinografia
Feminino
Substâncias Luminescentes/metabolismo
Luminol/análogos & derivados
Luminol/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Compressão Nervosa
Estresse Oxidativo
Reprodutibilidade dos Testes
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Luminescent Agents); 0 (Reactive Oxygen Species); 143323-55-1 (L 012); 5EXP385Q4F (Luminol)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170821
[Lr] Data última revisão:
170821
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170613
[St] Status:MEDLINE


  6 / 2428 MEDLINE  
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[PMID]:28587982
[Au] Autor:Somay H; Emon ST; Uslu S; Orakdogen M; Meric ZC; Ince U; Hakan T
[Ad] Endereço:Department of Neurosurgery, Haydarpasa Numune Training and Research Hospital, Istanbul, Turkey.
[Ti] Título:The Histological Effects of Ozone Therapy on Sciatic Nerve Crush Injury in Rats.
[So] Source:World Neurosurg;105:702-708, 2017 Sep.
[Is] ISSN:1878-8769
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Peripheral nerve injury is a common, important problem that lacks a definitive, effective treatment. It can cause neurologic deficits ranging from paresthesia to paralysis. This study evaluated the effect of ozone therapy on sciatic nerve crush injury in rats. MATERIALS AND METHODS: Twenty-four male rats were divided into control sham surgery, sciatic nerve injury, and sciatic nerve injury with ozone groups (each n = 8). The sciatic nerve injury was inflicted via De Koning's crush-force method. The sciatic nerve injury group received medical air and the sciatic nerve injury ozone group received 0.7 mg/kg ozone. Sciatic nerve samples were obtained 4 weeks after injury. Vascular congestion, vacuolization, edema formation, S100 expression, and the thicknesses of the perineurium and endoneurium and diameter of the injured sciatic nerves were evaluated. RESULTS: The diameter of the sciatic nerve and thicknesses of the perineurium and epineurium were significantly greater in the sciatic nerve injury group (P < 0.05) and significantly less in the sciatic nerve injury with ozone group (P < 0.001). High S100 immunoreactivity was seen in the sciatic nerve injury group compared with the other 2 groups (P < 0.05). The distributions of vascular congestion and vacuolization were significantly less in the sciatic nerve injury with ozone group (P < 0.05). CONCLUSIONS: Ozone therapy improved sciatic nerve injury recovery without causing an increase in fibrotic tissue. Ozone reduced fibrosis, vascular congestion, vacuolization, and edema in rodents. Ozone treatment might be used to assist in sciatic nerve injury.
[Mh] Termos MeSH primário: Compressão Nervosa/métodos
Ozônio/uso terapêutico
Neuropatia Ciática/tratamento farmacológico
Neuropatia Ciática/patologia
[Mh] Termos MeSH secundário: Animais
Masculino
Ratos
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
66H7ZZK23N (Ozone)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170608
[St] Status:MEDLINE


  7 / 2428 MEDLINE  
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[PMID]:28539419
[Au] Autor:Hilla AM; Diekmann H; Fischer D
[Ad] Endereço:Division of Experimental Neurology, Department of Neurology Medical Faculty, Heinrich-Heine-University, 40225 Düsseldorf, Germany.
[Ti] Título:Microglia Are Irrelevant for Neuronal Degeneration and Axon Regeneration after Acute Injury.
[So] Source:J Neurosci;37(25):6113-6124, 2017 Jun 21.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The role of microglia in degenerative and regenerative processes after damage of the nervous system remains ambiguous, partially due to the paucity of appropriate investigative methods. Here, we show that treatment with the pharmacological colony stimulating factor 1 receptor inhibitor PLX5622 specifically eliminated microglia in murine retinae and optic nerves with high efficiency. Interestingly, time course and extent of retinal ganglion cell (RGC) degeneration after optic nerve crush remained unaffected upon microglia depletion, although remnants of prelabeled apoptotic RGCs were not cleared from the retina in these animals. In addition, microglia depletion neither affected the induction of regeneration associated genes upon optic nerve injury nor the increased regenerative potential of RGCs upon lens injury (LI). However, although the repopulation of the optic nerve lesion site by astrocytes was significantly delayed upon microglia depletion, spontaneous and LI-induced axon regeneration were unaffected by PLX5622 treatment or peripheral macrophage depletion by clodronate liposome treatment. Only concurrent double depletion of microglia and infiltrated macrophages slightly, but significantly, compromised optic nerve regeneration. Therefore, microglia are not essentially involved in RGC degeneration or axonal regeneration after acute CNS injury. The roles of microglia, the phagocytosing cells of the CNS, and invading macrophages in degenerative and regenerative processes after injury are still controversial and insufficiently characterized. Here, we show that application of a CSF1R inhibitor eliminated virtually all microglia from the visual system, whereas macrophages were spared. Specific microglia depletion impaired the removal of dead labeled retinal ganglion cells after optic nerve crush, but remarkable had no influence on their degeneration. Similarly, optic nerve regeneration was completely unaffected, although repopulation of the lesion site by astrocytes was delayed significantly. Therefore, contrary to previous reports, this experimental approach revealed that microglia seemingly neither promote nor inhibit neuronal degeneration or axonal regrowth within the injured visual system.
[Mh] Termos MeSH primário: Axônios/patologia
Microglia/patologia
Degeneração Neural/patologia
Regeneração Nervosa
Traumatismos do Nervo Óptico/patologia
[Mh] Termos MeSH secundário: Animais
Astrócitos/patologia
Feminino
Cristalino/lesões
Cristalino/patologia
Macrófagos/efeitos dos fármacos
Macrófagos/patologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Compressão Nervosa
Receptores de Fator Estimulador de Colônias/antagonistas & inibidores
Retina/patologia
Células Ganglionares da Retina/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Colony-Stimulating Factor)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170814
[Lr] Data última revisão:
170814
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170526
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.0584-17.2017


  8 / 2428 MEDLINE  
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[PMID]:28441398
[Au] Autor:He T; Mortensen X; Wang P; Tian N
[Ad] Endereço:Eye Center Remin Hospital of Wuhan University Wuhan, Hubei, PR China.
[Ti] Título:The effects of immune protein CD3ζ development and degeneration of retinal neurons after optic nerve injury.
[So] Source:PLoS One;12(4):e0175522, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Major histocompatibility complex (MHC) class I molecules and their receptors play fundamental roles in neuronal death during diseases. T-cell receptors (TCR) function as MHCI receptor on T-cells and both MHCI and a key component of TCR, CD3ζ, are expressed by mouse retinal ganglion cells (RGCs) and displaced amacrine cells. Mutation of these molecules compromises the development of RGCs. We investigated whether CD3ζ regulates the development and degeneration of amacrine cells after RGC death. Surprisingly, mutation of CD3ζ not only impairs the proper development of amacrine cells expressing CD3ζ but also those not expressing CD3ζ. In contrast to effects of MHCI and its receptor, PirB, on other neurons, mutation of CD3ζ has no effect on RGC death and starburst amacrine cells degeneration after optic nerve crush. Thus, unlike MHCI and PirB, CD3ζ regulates the development of RGCs and amacrine cells but not their degeneration after optic nerve crush.
[Mh] Termos MeSH primário: Complexo CD3/imunologia
Traumatismos do Nervo Óptico/patologia
Nervo Óptico/patologia
Células Ganglionares da Retina/patologia
[Mh] Termos MeSH secundário: Células Amácrinas/imunologia
Células Amácrinas/patologia
Animais
Complexo CD3/genética
Morte Celular
Dendritos/imunologia
Dendritos/patologia
Camundongos Endogâmicos C57BL
Mutação
Compressão Nervosa
Nervo Óptico/citologia
Nervo Óptico/imunologia
Traumatismos do Nervo Óptico/genética
Traumatismos do Nervo Óptico/imunologia
Células Ganglionares da Retina/citologia
Células Ganglionares da Retina/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD3 Complex); 0 (CD3 antigen, zeta chain)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170426
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0175522


  9 / 2428 MEDLINE  
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Watanabe, Ii-Sei
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[PMID]:28314941
[Au] Autor:Martins DO; Dos Santos FM; Ciena AP; Watanabe IS; de Britto LRG; Lemos JBD; Chacur M
[Ad] Endereço:Department of Anatomy, Institute of Biomedical Sciences, University of São Paulo, Av. Prof. Lineu Prestes, 2415, São Paulo, SP, 05508-000, Brazil. martinsd@usp.br.
[Ti] Título:Neuropeptide expression and morphometric differences in crushed alveolar inferior nerve of rats: Effects of photobiomodulation.
[So] Source:Lasers Med Sci;32(4):833-840, 2017 May.
[Is] ISSN:1435-604X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Inferior alveolar nerve (IAN) injuries may occur during various dental routine procedures, especially in the removal of impacted lower third molars, and nerve recovery in these cases is a great challenge in dentistry. Here, the IAN crush injury model was used to assess the efficacy of photobiomodulation (PBM) in the recovery of the IAN in rats following crushing injury (a partial lesion). Rats were divided into four experimental groups: without any procedure, IAN crush injury, and IAN crush injury with PBM and sham group with PBM. Treatment was started 2 days after surgery, above the site of injury, and was performed every other day, totaling 10 sessions. Rats were irradiated with GaAs Laser (Gallium Arsenide, Laserpulse, Ibramed Brazil) emitting a wavelength of 904 nm, an output power of 70 mWpk, beam spot size at target ∼0.1 cm , a frequency of 9500 Hz, a pulse time 60 ns, and an energy density of 6 J/cm . Nerve recovery was investigated by measuring the morphometric data of the IAN using TEM and by the expression of laminin, neurofilaments (NFs), and myelin protein zero (MPZ) using Western blot analysis. We found that IAN-injured rats which received PBM had a significant improvement of IAN morphometry when compared to IAN-injured rats without PBM. In parallel, all MPZ, laminin, and NFs exhibited a decrease after PBM. The results of this study indicate that the correlation between the peripheral nerve ultrastructure and the associated protein expression shows the beneficial effects of PBM.
[Mh] Termos MeSH primário: Terapia com Luz de Baixa Intensidade
Nervo Mandibular/metabolismo
Nervo Mandibular/patologia
Compressão Nervosa
Neuropeptídeos/metabolismo
[Mh] Termos MeSH secundário: Animais
Densitometria
Filamentos Intermediários/metabolismo
Laminina/metabolismo
Masculino
Nervo Mandibular/ultraestrutura
Proteína P0 da Mielina/metabolismo
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Laminin); 0 (Myelin P0 Protein); 0 (Neuropeptides)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170319
[St] Status:MEDLINE
[do] DOI:10.1007/s10103-017-2181-2


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[PMID]:28265105
[Au] Autor:Maciulaitiene R; Pakuliene G; Kaja S; Pauza DH; Kalesnykas G; Januleviciene I
[Ad] Endereço:Department of Ophthalmology, Lithuanian University of Health Sciences, Academy of Medicine, Kaunas, Lithuania.
[Ti] Título:Glioprotection of Retinal Astrocytes After Intravitreal Administration of Memantine in the Mouse Optic Nerve Crush Model.
[So] Source:Med Sci Monit;23:1173-1179, 2017 Mar 07.
[Is] ISSN:1643-3750
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND In glaucoma, non-intraocular pressure (IOP)-related risk factors can result in increased levels of extracellular glutamate, which triggers a cascade of neurodegeneration characterized by the excessive activation of N-methyl-D-aspartate (NMDA). The purpose of our study was to evaluate the glioprotective effects of memantine as a prototypic uncompetitive NMDA blocker on retinal astrocytes in the optic nerve crush (ONC) mouse model for glaucoma. MATERIAL AND METHODS Optic nerve crush was performed on all of the right eyes (n=8), whereas left eyes served as contralateral healthy controls (n=8) in Balb/c/Sca mice. Four randomly assigned mice received 2-µl intravitreal injections of memantine (1 mg/ml) after ONC in the experimental eye. One week after the experiment, optic nerves were dissec-ted and stained with methylene blue. Retinae were detached from the sclera. The tissue was immunostained. Whole-mount retinae were investigated by fluorescent microscopy. Astrocyte counts for each image were performed manually. RESULTS Histological sections of crushed optic nerves showed consistently moderate tissue damage in experimental groups. The mean number of astrocytes per image in the ONC group was significantly lower than in the healthy control group (7.13±1.5 and 10.47±1.9, respectively). Loss of astrocytes in the memantine-treated group was significantly lower (8.83±2.2) than in the ONC group. Assessment of inter-observer reliability showed excellent agreement among observations in control, ONC, and memantine groups. CONCLUSIONS The ONC is an effective method for investigation of astrocytic changes in mouse retina. Intravitreally administered memantine shows a promising glioprotective effect on mouse retinal astrocytes by preserving astrocyte count after ONC.
[Mh] Termos MeSH primário: Astrócitos/patologia
Memantina/administração & dosagem
Memantina/farmacologia
Compressão Nervosa
Neuroglia/patologia
Neuroproteção/efeitos dos fármacos
Nervo Óptico/patologia
Retina/patologia
[Mh] Termos MeSH secundário: Animais
Astrócitos/efeitos dos fármacos
Astrócitos/metabolismo
Modelos Animais de Doenças
Proteína Glial Fibrilar Ácida/metabolismo
Injeções Intravítreas
Camundongos Endogâmicos BALB C
Neuroglia/efeitos dos fármacos
Neuroglia/metabolismo
Variações Dependentes do Observador
Retina/efeitos dos fármacos
Retina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glial Fibrillary Acidic Protein); W8O17SJF3T (Memantine)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170424
[Lr] Data última revisão:
170424
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170308
[St] Status:MEDLINE



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