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Pesquisa : D12.776.395.550.200.250.520.789 [Categoria DeCS]
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  1 / 22 MEDLINE  
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[PMID]:27880801
[Au] Autor:Chen W; Li YS; Gao J; Lin XY; Li XH
[Ad] Endereço:Department of Neurology, Jinan Central Hospital, Affiliated to Shandong University, Jinan, Shandong Province, China.
[Ti] Título:AMPA Receptor Antagonist NBQX Decreased Seizures by Normalization of Perineuronal Nets.
[So] Source:PLoS One;11(11):e0166672, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Epilepsy is a serious brain disorder with diverse seizure types and epileptic syndromes. AMPA receptor antagonist 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzoquinoxaline-2,3-dione (NBQX) attenuates spontaneous recurrent seizures in rats. However, the anti-epileptic effect of NBQX in chronic epilepsy model is poorly understood. Perineuronal nets (PNNs), specialized extracellular matrix structures, surround parvalbumin-positive inhibitory interneurons, and play a critical role in neuronal cell development and synaptic plasticity. Here, we focused on the potential involvement of PNNs in the treatment of epilepsy by NBQX. Rats were intraperitoneally (i.p.) injected with pentylenetetrazole (PTZ, 50 mg/kg) for 28 consecutive days to establish chronic epilepsy models. Subsequently, NBQX (20 mg/kg, i.p.) was injected for 3 days for the observation of behavioral measurements of epilepsy. The Wisteria floribundi agglutinin (WFA)-labeled PNNs were measured by immunohistochemical staining to evaluate the PNNs. The levels of three components of PNNs such as tenascin-R, aggrecan and neurocan were assayed by Western blot assay. The results showed that there are reduction of PNNs and decrease of tenascin-R, aggrecan and neurocan in the medial prefrontal cortex (mPFC) in the rats injected with PTZ. However, NBQX treatment normalized PNNs, tenascin-R, aggrecan and neurocan levels. NBQX was sufficient to decrease seizures through increasing the latency to seizures, decrease the duration of seizure onset, and reduce the scores for the severity of seizures. Furthermore, the degradation of mPFC PNNs by chondroitinase ABC (ChABC) exacerbated seizures in PTZ-treated rats. Finally, the anti-epileptic effect of NBQX was reversed by pretreatment with ChABC into mPFC. These findings revealed that PNNs degradation in mPFC is involved in the pathophysiology of epilepsy and enhancement of PNNs may be effective for the treatment of epilepsy.
[Mh] Termos MeSH primário: Anticonvulsivantes/farmacologia
Epilepsia/prevenção & controle
Nervos Periféricos/efeitos dos fármacos
Quinoxalinas/farmacologia
Receptores de AMPA/antagonistas & inibidores
[Mh] Termos MeSH secundário: Agrecanas/metabolismo
Animais
Anticonvulsivantes/uso terapêutico
Comportamento Animal/efeitos dos fármacos
Condroitina ABC Liase/farmacologia
Modelos Animais de Doenças
Regulação para Baixo/efeitos dos fármacos
Epilepsia/induzido quimicamente
Epilepsia/patologia
Imuno-Histoquímica
Masculino
Neurocam/metabolismo
Pentilenotetrazol/toxicidade
Nervos Periféricos/metabolismo
Córtex Pré-Frontal/metabolismo
Quinoxalinas/uso terapêutico
Ratos
Ratos Wistar
Receptores de AMPA/metabolismo
Tenascina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aggrecans); 0 (Anticonvulsants); 0 (Neurocan); 0 (Quinoxalines); 0 (Receptors, AMPA); 0 (Tenascin); 118876-58-7 (2,3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxaline); 147604-77-1 (tenascin R); EC 4.2.2.20 (Chondroitin ABC Lyase); WM5Z385K7T (Pentylenetetrazole)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170627
[Lr] Data última revisão:
170627
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161124
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0166672


  2 / 22 MEDLINE  
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[PMID]:27317830
[Au] Autor:Yan H; Zhu X; Xie J; Zhao Y; Liu X
[Ad] Endereço:Department of Neurology, Shanghai Tenth People's Hospital, Tongji University, School of Medicine, 301 Middle Yanchang Road, Shanghai 200072, PR China.
[Ti] Título:ß-amyloid increases neurocan expression through regulating Sox9 in astrocytes: A potential relationship between Sox9 and chondroitin sulfate proteoglycans in Alzheimer's disease.
[So] Source:Brain Res;1646:377-383, 2016 Sep 01.
[Is] ISSN:1872-6240
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: This study aimed to investigate whether ß-amyloid (Aß) was able to enhance neurocan expression in a Sox9 dependent manner in astrocytes. METHODS AND MATERIALS: Astrocytes were incubated with Aß at different concentrations, the expression of Sox9 and neurocan was detected by Western blot assay. Meanwhile, the viability and proliferation of astrocytes were assessed by MTT assay. Then, the Sox9 expression was silenced, and the expression of Sox9 and neurocan was examined. RESULTS: After incubation with Aß, the viability of astrocytes was increased regardless silencing of Sox9 (all P<0.05). The proliferation of astrocytes was also gradually increased with the increase in the time of Aß incubation (all P<0.05). With the increase in Aß concentration, the expression of Sox9 and neurocan was also increased (all P<0.05). However, after silencing of Sox9 expression, the neurocan expression was significantly reduced as compared to control group and scra-siRNA group (all P<0.05). CONCLUSION: Our study shows the viability and proliferation of astrocytes are significantly increased by Aß in a dose dependent manner. Moreover, Aß may effectively up-regulate the neurocan expression via regulating Sox9.
[Mh] Termos MeSH primário: Doença de Alzheimer/metabolismo
Peptídeos beta-Amiloides/administração & dosagem
Astrócitos/metabolismo
Neurocam/metabolismo
Fragmentos de Peptídeos/administração & dosagem
Fatores de Transcrição SOX9/metabolismo
[Mh] Termos MeSH secundário: Animais
Proliferação Celular
Sobrevivência Celular
Células Cultivadas
Proteoglicanas de Sulfatos de Condroitina/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
RNA Mensageiro/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amyloid beta-Peptides); 0 (Chondroitin Sulfate Proteoglycans); 0 (Neurocan); 0 (Peptide Fragments); 0 (RNA, Messenger); 0 (SOX9 Transcription Factor); 0 (Sox9 protein, mouse); 0 (amyloid beta-protein (1-42))
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170806
[Lr] Data última revisão:
170806
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160619
[St] Status:MEDLINE


  3 / 22 MEDLINE  
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[PMID]:27006005
[Au] Autor:Zhang J; Wang H; Zhang C; Li W
[Ad] Endereço:No.1 Department of Orthopedic Surgery, Tianjin Baodi Hospital, No.8, Guangchuan Road, Baodi District, Tianjin, 301800, China. zhajian@umich.edu.
[Ti] Título:Intrathecal decompression versus epidural decompression in the treatment of severe spinal cord injury in rat model: a randomized, controlled preclinical research.
[So] Source:J Orthop Surg Res;11:34, 2016 Mar 22.
[Is] ISSN:1749-799X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: In the setting of severe spinal cord injury (SCI), there is no markedly efficacious clinical therapeutic regimen to improve neurological function. After epidural decompression, as is shown in animal models, the swollen cord against non-elastic dura and elevation of intrathecal pressure may be the main causes of aggravated neurologic function. We performed an intrathecal decompression by longitudinal durotomy to evaluate the neuroprotective effect after severe SCI by comparing with epidural decompression. METHODS: Eighty-four adult male Sprague-Dawley rats were assigned to three groups: sham group (group S), epidural decompression (group C), and intrathecal decompression group (group D). A weight-drop model was performed at T9. The Basso-Beattie-Bresnahan (BBB) score was used to evaluate neurological function. Animals were sacrificed at corresponding time points, and we performed pathohistological examinations including HE staining and immunohistochemical staining (IHC) of glial fibrillary acidic protein (GFAP), neurocan, and ED1 at the epicenter of injured cords. Finally, the lesions were quantitatively analyzed by SPSS 22.0. RESULTS: The mortality rates were, respectively, 5.55 % (2/36) and 13.9 % (5/36) in groups C and D, and there was no significant difference between groups C and D (P = 0.214). Compared with epidural decompression, intrathecal decompression could obviously improve BBB scores after SCI. HE staining indicated that more white matter was spared, and fewer vacuoles and less axon degradation were observed. The expression peak of GFAP, neurocan, and ED1 occurred at an earlier time and was down-regulated in group D compared to group C. CONCLUSIONS: Our findings based on rat SCI model suggest that intrathecal decompression by longitudinal durotomy can prompt recovery of neurological function, and this neuroprotective mechanism may be related to the down-regulation of GFAP, neurocan, and ED1.
[Mh] Termos MeSH primário: Descompressão Cirúrgica/métodos
Traumatismos da Medula Espinal/cirurgia
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Dura-Máter/cirurgia
Ectodisplasinas/metabolismo
Espaço Epidural
Proteína Glial Fibrilar Ácida/metabolismo
Masculino
Atividade Motora
Neurocam/metabolismo
Distribuição Aleatória
Ratos Sprague-Dawley
Recuperação de Função Fisiológica
Traumatismos da Medula Espinal/metabolismo
Traumatismos da Medula Espinal/patologia
Traumatismos da Medula Espinal/fisiopatologia
Análise de Sobrevida
[Pt] Tipo de publicação:COMPARATIVE STUDY; EVALUATION STUDIES; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Ectodysplasins); 0 (Glial Fibrillary Acidic Protein); 0 (Neurocan)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160324
[St] Status:MEDLINE
[do] DOI:10.1186/s13018-016-0369-y


  4 / 22 MEDLINE  
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[PMID]:26322652
[Au] Autor:Xu X; Li N; Zhu L; Zhou Y; Cheng H
[Ad] Endereço:a Department of Neurosurgery , Jinling Hospital, School of Medicine, Nanjing University , Nanjing , Jiangsu Province , China.
[Ti] Título:Beneficial effects of local profound hypothermia and the possible mechanism after experimental spinal cord injury in rats.
[So] Source:J Spinal Cord Med;39(2):220-8, 2016.
[Is] ISSN:2045-7723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: The primary focus of this study was to investigate the effects of local profound hypothermia and to explore the possible mechanism in adult rats with spinal cord injury. STUDY DESIGN AND METHODS: Spinal cord injury models were established by placing aneurysm clips on T10. An epidural perfusion device was applied to maintain a steady temperature (18 °C) for 120 min with gradual rewarming to 37 °C Total hypothermic duration lasted up to about 170 min. The expression of axon regeneration inhibitors was tested by Western blot and real-time PCR. Luxol Fast Blue (LFB) stain and Bielschowsky silver stain were used to observe spinal cord morphology. Motor function of the hind limbs (BBB score) was monitored for 21 days. RESULTS: The expressions of RhoA, ROCK-II, NG2, Neurocan, Brevican, and Nogo-A were downregulated by regional hypothermia (RH) after spinal cord injury. Subsequent observation showed that rats that had received RH had an alleviated demyelinating condition and a greater number of nerve fibers. Furthermore, the RH group achieved higher BBB scores than the spinal cord injury (SCI) group. CONCLUSIONS: Recovery of hind limb function in rats can be promoted by local profound hypothermia; this may be caused by the suppression of axon regeneration inhibitors.
[Mh] Termos MeSH primário: Hipotermia Induzida
Regeneração Nervosa
Traumatismos da Medula Espinal/terapia
[Mh] Termos MeSH secundário: Animais
Axônios/metabolismo
Axônios/fisiologia
Brevicam/genética
Brevicam/metabolismo
Regulação para Baixo
Membro Posterior/inervação
Membro Posterior/fisiologia
Masculino
Neurocam/genética
Neurocam/metabolismo
Proteínas Nogo/genética
Proteínas Nogo/metabolismo
Ratos
Ratos Sprague-Dawley
Recuperação de Função Fisiológica
Traumatismos da Medula Espinal/reabilitação
Quinases Associadas a rho/genética
Quinases Associadas a rho/metabolismo
Proteína rhoA de Ligação ao GTP/genética
Proteína rhoA de Ligação ao GTP/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Brevican); 0 (Neurocan); 0 (Nogo Proteins); EC 2.7.11.1 (rho-Associated Kinases); EC 3.6.5.2 (rhoA GTP-Binding Protein)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170301
[Lr] Data última revisão:
170301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150901
[St] Status:MEDLINE
[do] DOI:10.1179/2045772315Y.0000000051


  5 / 22 MEDLINE  
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[PMID]:26729092
[Au] Autor:Ye L; Yang Y; Zhang X; Cai P; Li R; Chen D; Wei X; Zhang X; Xu H; Xiao J; Li X; Lin L; Zhang H
[Ad] Endereço:Key Laboratory of Biotechnology and Pharmaceutical Engineering, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou 325035, China. wzlbye@126.com.
[Ti] Título:The Role of bFGF in the Excessive Activation of Astrocytes Is Related to the Inhibition of TLR4/NFκB Signals.
[So] Source:Int J Mol Sci;17(1), 2015 Dec 28.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Astrocytes have critical roles in immune defense, homeostasis, metabolism, and synaptic remodeling and function in the central nervous system (CNS); however, excessive activation of astrocytes with increased intermediate filaments following neuronal trauma, infection, ischemia, stroke, and neurodegenerative diseases results in a pro-inflammatory environment and promotes neuronal death. As an important neurotrophic factor, the secretion of endogenous basic fibroblast growth factor (bFGF) contributes to the protective effect of neuronal cells, but the mechanism of bFGF in reactive astrogliosis is still unclear. In this study, we demonstrated that exogenous bFGF attenuated astrocyte activation by reducing the expression of glial fibrillary acidic protein (GFAP) and other markers, including neurocan and vimentin, but not nestin and decreased the levels of pro-inflammatory cytokines, such as interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), via the regulation of the upstream toll-like receptor 4/nuclear factor κB (TLR4/NFκB) signaling pathway. Our study suggests that the function of bFGF is not only related to the neuroprotective and neurotrophic effect but also involved in the inhibition of excessive astrogliosis and glial scarring after neuronal injury.
[Mh] Termos MeSH primário: Astrócitos/patologia
Fator 2 de Crescimento de Fibroblastos/fisiologia
Gliose/fisiopatologia
NF-kappa B
Transdução de Sinais
Receptor 4 Toll-Like
[Mh] Termos MeSH secundário: Animais
Astrócitos/metabolismo
Astrócitos/fisiologia
Células Cultivadas
Citocinas/genética
Regulação para Baixo
Proteína Glial Fibrilar Ácida/genética
Gliose/metabolismo
Neurocam/genética
Ratos
Vimentina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cytokines); 0 (Glial Fibrillary Acidic Protein); 0 (NF-kappa B); 0 (Neurocan); 0 (Tlr4 protein, rat); 0 (Toll-Like Receptor 4); 0 (Vimentin); 103107-01-3 (Fibroblast Growth Factor 2)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160106
[St] Status:MEDLINE


  6 / 22 MEDLINE  
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[PMID]:24561092
[Au] Autor:Pócsai K; Kálmán M
[Ad] Endereço:Department of Anatomy, Histology and Embryology, Semmelweis University, Tuzolto 58, Budapest, H-1094 Hungary. Electronic address: pocsai.karoly@gmail.com.
[Ti] Título:Extracellular matrix components mark the territories of circumventricular organs.
[So] Source:Neurosci Lett;566:36-41, 2014 Apr 30.
[Is] ISSN:1872-7972
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:In the central nervous system the extracellular matrix has important roles, e.g. supporting the extracellular space, controlling the tissue hydration, binding soluble factors and influencing their diffusion. The distribution of the extracellular matrix components in the brain has been mapped but data on the circumventricular organs (CVOs) is not available yet. The CVOs lack the blood-brain barrier and have relatively large perivascular spaces. The present study investigates tenascin-R and the lecticans: aggrecan, brevican, neurocan, and versican in the median eminence, the area postrema, the vascular organ of the lamina terminalis, the subfornical organ, the pineal body and the subcommissural organ of the rat applying immunohistochemical methods, and lectin histochemistry, using Wisteria floribunda agglutinin (WFA). The extracellular matrix components were found intensely expressed in the CVOs with two exceptions: aggrecan immunoreactivity visualized only neurons in the arcuate nucleus, and the subcommissural organ was not labeled with either WFA, or lecticans, or tenascin-R. The different labelings usually overlapped each other. The distribution of the extracellular matrix components marked the territories of the CVOs. Considering these we suppose that the extracellular matrix is essential in the maintenance of CVO functions providing the large extracellular space which is required for diffusion and other processes important in their chemosensitive and neurosecretory activities. The decrease of extracellular matrix beyond the border of the organs may contribute to the control of the diffusion of molecules from the CVOs into the surrounding brain substance.
[Mh] Termos MeSH primário: Área Postrema/metabolismo
Proteínas da Matriz Extracelular/metabolismo
Hipotálamo/metabolismo
Eminência Mediana/metabolismo
Sistemas Neurossecretores/metabolismo
[Mh] Termos MeSH secundário: Agrecanas/metabolismo
Animais
Brevicam/metabolismo
Feminino
Masculino
Neurocam/metabolismo
Glândula Pineal/metabolismo
Ratos Wistar
Órgão Subcomissural/metabolismo
Órgão Subfornical/metabolismo
Tenascina/metabolismo
Versicanas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Aggrecans); 0 (Brevican); 0 (Extracellular Matrix Proteins); 0 (Neurocan); 0 (Tenascin); 126968-45-4 (Versicans); 147604-77-1 (tenascin R)
[Em] Mês de entrada:1411
[Cu] Atualização por classe:140415
[Lr] Data última revisão:
140415
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140225
[St] Status:MEDLINE


  7 / 22 MEDLINE  
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[PMID]:24519742
[Au] Autor:Yu CY; Gui W; He HY; Wang XS; Zuo J; Huang L; Zhou N; Wang K; Wang Y
[Ad] Endereço:Epilepsy and Headache Group, Department of Neurology, The First Hospital of Anhui Medical University, Jixi Road 218, Hefei, 230022, China.
[Ti] Título:Neuronal and astroglial TGFß-Smad3 signaling pathways differentially regulate dendrite growth and synaptogenesis.
[So] Source:Neuromolecular Med;16(2):457-72, 2014 Jun.
[Is] ISSN:1559-1174
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:To address the role of the transforming growth factor beta (TGFß)-Smad3 signaling pathway in dendrite growth and associated synaptogenesis, we used small inhibitory RNA to knockdown the Smad3 gene in either cultured neurons and or primary astrocytes. We found that TGFß1 treatment of primary neurons increased dendrite extensions and the number of synapsin-1-positive synapses. When Smad3 was knockdown in primary neurons, dendrite growth was inhibited and the number of synapsin-1-positive synapses reduced even with TGFß1 treatment. When astrocyte-conditioned medium (ACM), collected from TGFß1-treated astrocytes (TGFß1-stimulated ACM), was added to cultured neurons, dendritic growth was inhibited and the number of synapsin-1-positive puncta reduced. When TGFß1-stimulated ACM was collected from astrocytes with Smad3 knocked down, this conditioned media promoted the growth of dendrites and the number of synapsin-1-positive puncta in cultured neurons. We further found that TGFß1 signaling through Smad3 increased the expression of chondroitin sulfate proteoglycans, neurocan, and phosphacan in ACM. Application of chondroitinase ABC to the TGFß1-stimulated ACM reversed its inhibitory effects on the dendrite growth and the number of synapsin-1-positive puncta. On the other hand, we found that TGFß1 treatment caused a facilitation of Smad3 phosphorylation and translocation to the nucleus induced by status epilepticus (SE) in wild-type (Smad3(+/+)) mice, and this treatment also caused a promotion of γ-aminobutyric acid-ergic synaptogenesis impaired by SE in Smad3(+/+) as well as in Smad3(-/-) mice, but more dramatic promotion in Smad3(+/+) mice. Thus, we provide evidence for the first time that TGFß-Smad3 signaling pathways within neuron and astrocyte differentially regulate dendrite growth and synaptogenesis, and this pathway may be involved in the pathogenesis of some central nervous system diseases, such as epilepsy.
[Mh] Termos MeSH primário: Astrócitos/metabolismo
Neurônios/metabolismo
Transdução de Sinais/fisiologia
Proteína Smad3/fisiologia
Sinapses/ultraestrutura
Fator de Crescimento Transformador beta1/fisiologia
[Mh] Termos MeSH secundário: Transporte Ativo do Núcleo Celular
Animais
Astrócitos/efeitos dos fármacos
Astrócitos/ultraestrutura
Células Cultivadas
Condroitina ABC Liase/farmacologia
Proteoglicanas de Sulfatos de Condroitina/biossíntese
Proteoglicanas de Sulfatos de Condroitina/genética
Meios de Cultivo Condicionados/farmacologia
Feminino
Regulação da Expressão Gênica
Masculino
Camundongos
Camundongos Endogâmicos ICR
Camundongos Knockout
Neurocam/biossíntese
Neurocam/genética
Neurônios/ultraestrutura
Processamento de Proteína Pós-Traducional/efeitos dos fármacos
Interferência de RNA
RNA Interferente Pequeno/farmacologia
Proteínas Tirosina Fosfatases Classe 5 Semelhantes a Receptores/biossíntese
Proteínas Tirosina Fosfatases Classe 5 Semelhantes a Receptores/genética
Proteína Smad3/antagonistas & inibidores
Proteína Smad3/deficiência
Proteína Smad3/genética
Estado Epiléptico/metabolismo
Sinapsinas/análise
Fator de Crescimento Transformador beta1/farmacologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Chondroitin Sulfate Proteoglycans); 0 (Culture Media, Conditioned); 0 (Neurocan); 0 (RNA, Small Interfering); 0 (Smad3 Protein); 0 (Smad3 protein, mouse); 0 (Synapsins); 0 (Transforming Growth Factor beta1); EC 3.1.3.48 (Receptor-Like Protein Tyrosine Phosphatases, Class 5); EC 4.2.2.20 (Chondroitin ABC Lyase)
[Em] Mês de entrada:1501
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140213
[St] Status:MEDLINE
[do] DOI:10.1007/s12017-014-8293-y


  8 / 22 MEDLINE  
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[PMID]:24462452
[Au] Autor:Wright KT; Uchida K; Bara JJ; Roberts S; El Masri W; Johnson WE
[Ad] Endereço:Centre for Spinal Studies, Robert Jones and Agnes Hunt Orthopaedic Hospital, Oswestry, Shropshire SY10 7AG, UK; Institute for Science and Technology in Medicine, Keele University, Keele, Staffordshire ST5 5BG, UK. Electronic address: Karina.Wright@rjah.nhs.uk.
[Ti] Título:Spinal motor neurite outgrowth over glial scar inhibitors is enhanced by coculture with bone marrow stromal cells.
[So] Source:Spine J;14(8):1722-33, 2014 Aug 01.
[Is] ISSN:1878-1632
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND CONTEXT: Transplantation of bone marrow cells into spinal cord lesions promotes functional recovery in animal models, and recent clinical trials suggest possible recovery also in humans. The mechanisms responsible for these improvements are still unclear. PURPOSE: To characterize spinal cord motor neurite interactions with human bone marrow stromal cells (MSCs) in an in vitro model of spinal cord injury (SCI). STUDY DESIGN/SETTING: Previously, we have reported that human MSCs promote the growth of extending sensory neurites from dorsal root ganglia (DRG), in the presence of some of the molecules present in the glial scar, which are attributed with inhibiting axonal regeneration after SCI. We have adapted and optimized this system replacing the DRG with a spinal cord culture to produce a central nervous system (CNS) model, which is more relevant to the SCI situation. METHODS: We have developed and characterized a novel spinal cord culture system. Human MSCs were cocultured with spinal motor neurites in substrate choice assays containing glial scar-associated inhibitors of nerve growth. In separate experiments, MSC-conditioned media were analyzed and added to spinal motor neurites in substrate choice assays. RESULTS: As has been reported previously with DRG, substrate-bound neurocan and Nogo-A repelled spinal neuronal adhesion and neurite outgrowth, but these inhibitory effects were abrogated in MSC/spinal cord cocultures. However, unlike DRG, spinal neuronal bodies and neurites showed no inhibition to substrates of myelin-associated glycoprotein. In addition, the MSC secretome contained numerous neurotrophic factors that stimulated spinal neurite outgrowth, but these were not sufficient stimuli to promote spinal neurite extension over inhibitory concentrations of neurocan or Nogo-A. CONCLUSIONS: These findings provide novel insight into how MSC transplantation may promote regeneration and functional recovery in animal models of SCI and in the clinic, especially in the chronic situation in which glial scars (and associated neural inhibitors) are well established. In addition, we have confirmed that this CNS model predominantly comprises motor neurons via immunocytochemical characterization. We hope that this model may be used in future research to test various other potential interventions for spinal injury or disease states.
[Mh] Termos MeSH primário: Células Mesenquimais Estromais/citologia
Neurônios Motores/citologia
Neuritos/fisiologia
[Mh] Termos MeSH secundário: Adulto
Animais
Embrião de Galinha
Técnicas de Cocultura
Seres Humanos
Células Mesenquimais Estromais/efeitos dos fármacos
Células Mesenquimais Estromais/fisiologia
Meia-Idade
Neurônios Motores/efeitos dos fármacos
Neurônios Motores/fisiologia
Proteínas da Mielina/farmacologia
Neuritos/efeitos dos fármacos
Neurocam/farmacologia
Proteínas Nogo
Traumatismos da Medula Espinal/fisiopatologia
Traumatismos da Medula Espinal/terapia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Myelin Proteins); 0 (Neurocan); 0 (Nogo Proteins); 0 (RTN4 protein, human)
[Em] Mês de entrada:1510
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140128
[St] Status:MEDLINE


  9 / 22 MEDLINE  
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[PMID]:24460490
[Au] Autor:Mahmood A; Wu H; Qu C; Mahmood S; Xiong Y; Kaplan DL; Chopp M
[Ad] Endereço:Departments of Neurosurgery and.
[Ti] Título:Suppression of neurocan and enhancement of axonal density in rats after treatment of traumatic brain injury with scaffolds impregnated with bone marrow stromal cells.
[So] Source:J Neurosurg;120(5):1147-55, 2014 May.
[Is] ISSN:1933-0693
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECT: Neurocan is a major form of growth-inhibitory molecule (growth-IM) that suppresses axonal regeneration after neural injury. Bone marrow stromal cells (MSCs) have been shown to inhibit neurocan expression in vitro and in animal models of cerebral ischemia. Therefore, the present study was designed to investigate the effects of treatment of MSCs impregnated with collagen scaffolds on neurocan expression after traumatic brain injury (TBI). METHODS: Adult male Wistar rats were injured with controlled cortical impact and treated with saline, human MSCs (hMSCs) (3 × 10(6)) alone, or hMSCs (3 × 10(6)) impregnated into collagen scaffolds (scaffold + hMSCs) transplanted into the lesion cavity 7 days after TBI (20 rats per group). Rats were sacrificed 14 days after TBI, and brain tissues were harvested for immunohistochemical studies, Western blot analyses, laser capture microdissections, and quantitative real-time reverse transcriptase polymerase chain reaction (qRT-PCR) to evaluate neurocan protein and gene expressions after various treatments. RESULTS: Animals treated with scaffold + hMSCs after TBI showed increased axonal and synaptic densities compared with the other groups. Scaffold + hMSC treatment was associated with reduced TBI-induced neurocan protein expression and upregulated growth-associated protein 43 (GAP-43) and synaptophysin expression in the lesion boundary zone. In addition, animals in the scaffold + hMSC group had decreased neurocan transcription in reactive astrocytes after TBI. Reduction of neurocan expression was significantly greater in the scaffold + hMSC group than in the group treated with hMSCs alone. CONCLUSIONS: The results of this study show that transplanting hMSCs with scaffolds enhances the effect of hMSCs on axonal plasticity in TBI rats. This enhanced axonal plasticity may partially be attributed to the downregulation of neurocan expression by hMSC treatment after injury.
[Mh] Termos MeSH primário: Axônios/metabolismo
Lesões Encefálicas/terapia
Transplante de Células-Tronco Mesenquimais
Células Mesenquimais Estromais/metabolismo
Neurocam/metabolismo
Tecidos Suporte
[Mh] Termos MeSH secundário: Animais
Axônios/patologia
Lesões Encefálicas/metabolismo
Lesões Encefálicas/patologia
Colágeno/metabolismo
Modelos Animais de Doenças
Masculino
Ratos
Ratos Wistar
Recuperação de Função Fisiológica/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neurocan); 9007-34-5 (Collagen)
[Em] Mês de entrada:1407
[Cu] Atualização por classe:140505
[Lr] Data última revisão:
140505
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:140128
[St] Status:MEDLINE
[do] DOI:10.3171/2013.12.JNS131362


  10 / 22 MEDLINE  
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[PMID]:23681169
[Au] Autor:Rácz E; Gaál B; Kecskes S; Matesz C
[Ad] Endereço:Department of Anatomy, Histology and Embryology, Faculty of Medicine, Medical and Health Science Center, University of Debrecen, Nagyerdei krt. 98, Debrecen, 4032, Hungary.
[Ti] Título:Molecular composition of extracellular matrix in the vestibular nuclei of the rat.
[So] Source:Brain Struct Funct;219(4):1385-403, 2014 Jul.
[Is] ISSN:1863-2661
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Previous studies have demonstrated that the molecular and structural composition of the extracellular matrix (ECM) shows regional differences in the central nervous system. By using histochemical and immunohistochemical methods, we provide here a detailed map of the distribution of ECM molecules in the vestibular nuclear complex (VNC) of the rat. We have observed common characteristics of the ECM staining pattern in the VNC and a number of differences among the individual vestibular nuclei and their subdivisions. The perineuronal net (PNN), which is the pericellular condensation of ECM, showed the most intense staining for hyaluronan, aggrecan, brevican and tenascin-R in the superior, lateral and medial vestibular nuclei, whereas the HAPLN1 link protein and the neurocan exhibited moderate staining intensity. The rostral part of the descending vestibular nucleus (DVN) presented a similar staining pattern in the PNN, with the exception of brevican, which was negative. The caudal part of the DVN had the weakest staining for all ECM molecules in the PNN. Throughout the VNC, versican staining in the PNN, when present, was distinctive due to its punctuate appearance. The neuropil also exhibited heterogeneity among the individual vestibular nuclei in ECM staining pattern and intensity. We find that the heterogeneous distribution of ECM molecules is associated in many cases with the variable cytoarchitecture and hodological organization of the vestibular nuclei, and propose that differences in the ECM composition may be related to specific neuronal functions associated with gaze and posture control and vestibular compensation.
[Mh] Termos MeSH primário: Matriz Extracelular/metabolismo
Neurônios/metabolismo
Neurópilo/metabolismo
Núcleos Vestibulares/metabolismo
[Mh] Termos MeSH secundário: Agrecanas/metabolismo
Animais
Brevicam/metabolismo
Proteínas da Matriz Extracelular/metabolismo
Feminino
Ácido Hialurônico/metabolismo
Neurocam/metabolismo
Proteoglicanas/metabolismo
Ratos
Ratos Wistar
Tenascina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Aggrecans); 0 (Brevican); 0 (Extracellular Matrix Proteins); 0 (Neurocan); 0 (Proteoglycans); 0 (Tenascin); 0 (link protein); 147604-77-1 (tenascin R); 9004-61-9 (Hyaluronic Acid)
[Em] Mês de entrada:1502
[Cu] Atualização por classe:140626
[Lr] Data última revisão:
140626
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130518
[St] Status:MEDLINE
[do] DOI:10.1007/s00429-013-0575-x



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