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[PMID]:27772534
[Au] Autor:Keshavarz M
[Ad] Endereço:Shiraz Neuroscience Research Center,Shiraz University of Medical Sciences,Shiraz,Iran.
[Ti] Título:Glial cells as key elements in the pathophysiology and treatment of bipolar disorder.
[So] Source:Acta Neuropsychiatr;29(3):140-152, 2017 Jun.
[Is] ISSN:1601-5215
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: The exact pathophysiology of bipolar disorder (BD) is not yet fully understood, and there are many questions in this area which should be answered. This review aims to discuss the roles of glial cells in the pathophysiology of BD and their contribution to the mechanism of action of mood-stabilising drugs. METHODS: We critically reviewed the most recent advances regarding glial cell roles in the pathophysiology and treatment of BD and the neuroprotective and neurotrophic effects of these cells. RESULTS: Postmortem studies revealed a decrease in the glial cell number or density in the specific layers of prefrontal and anterior cingulate cortex in the patients with BD, whereas there was no difference in other brain regions, such as entorhinal cortex, amygdala and hippocampus. Astrocytes and oligodendrocytes were the most important glial types that were responsible for the glial reduction, but microglia activation rather than loss may be implicated in BD. The decreased number or density of glial cells may contribute to the pathological changes observed in neurons in the patients with BD. Alteration of specific neurotrophic factors such as glial cell line-derived neurotrophic factor and S100B may be an important feature of BD. Glial cells mediate the therapeutic effects of mood-stabilising agents in the treatment of BD. CONCLUSION: Recent studies provide important evidence on the impairment of glial cells in the pathophysiology and treatment of BD. However, future controlled studies are necessary to elucidate different aspects of glial cells contribution to BD, and the mechanism of action of mood-stabilising drugs.
[Mh] Termos MeSH primário: Tonsila do Cerebelo/citologia
Transtorno Bipolar/fisiopatologia
Hipocampo/citologia
Neuroglia/fisiologia
[Mh] Termos MeSH secundário: Tonsila do Cerebelo/metabolismo
Tonsila do Cerebelo/patologia
Astrócitos/metabolismo
Astrócitos/patologia
Transtorno Bipolar/tratamento farmacológico
Encéfalo/patologia
Encéfalo/fisiopatologia
Diagnóstico
Fator Neurotrófico Derivado de Linhagem de Célula Glial/metabolismo
Hipocampo/metabolismo
Hipocampo/patologia
Seres Humanos
Transtornos do Humor/tratamento farmacológico
Neuroglia/citologia
Neuroglia/metabolismo
Neurônios/metabolismo
Neurônios/patologia
Oligodendroglia/metabolismo
Oligodendroglia/patologia
Subunidade beta da Proteína Ligante de Cálcio S100/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (GDNF protein, human); 0 (Glial Cell Line-Derived Neurotrophic Factor); 0 (S100 Calcium Binding Protein beta Subunit); 0 (S100B protein, human)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1017/neu.2016.56


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[PMID]:29307828
[Au] Autor:Wang X; Min S; Xie F; Yang J; Li L; Chen J
[Ad] Endereço:Department of Anesthesiology, First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
[Ti] Título:Glial cell-derived neurotrophic factor alleviates sepsis-induced neuromuscular dysfunction by decreasing the expression of γ- and α7-nicotinic acetylcholine receptors in an experimental rat model of neuromyopathy.
[So] Source:Biochem Biophys Res Commun;496(2):260-266, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sepsis-induced neuromuscular dysfunction results from up-regulation of the expression of γ- and α7-nicotinic acetylcholine receptors (nAChR). Although glial cell derived neurotrophic factor (GDNF) has been implicated in repairing and supporting neurons, little is known about the effects of GDNF on demyelination of nerves in sepsis. In this study, we tested the hypothesis that GDNF could alleviate sepsis-induced neuromuscular dysfunction by decreasing the expression of γ- and α7-nAChR in an experimental rat model of neuromyopathy. Rats were randomly divided into a sham group and a sepsis group. Levels of inflammatory factors, muscle function, and nicotinic acetylcholine receptors were tested in rats after cecal ligation and puncture (CLP). At 24 h after CLP, GDNF was injected around the sciatic nerve of sepsis rats, cytokines were detected by enzyme-linked immunosorbent assay (ELISA), and immunofluorescence staining was used to detect the expression of nAChRs. GDNF and its downstream effector (Erk1/2 and GFR-α), neuregulin-1 (NRG-1) and γ- and α7-nAChR were measured using Western blot analysis. The expression of GDNF reached a minimum at 24 h after CLP. Compared with the sham group, the release of cytokines and the expression of γ- and α7-nAChR were significantly increased in the sepsis group. The administration of GDNF significantly alleviated sepsis-induced neuromuscular dysfunction, as well as reducing the expression of γ- and α7-nAChR. In addition, the expression of Erk1/2, GFR-α, NRG-1 were significantly increased after GDNF treatment. GDNF administration may improve patient outcomes by reducing the demyelination of nerves and the expression of γ- and α7-nAChR.
[Mh] Termos MeSH primário: Anti-Inflamatórios/farmacologia
Doenças Desmielinizantes/tratamento farmacológico
Fator Neurotrófico Derivado de Linhagem de Célula Glial/farmacologia
Doenças Musculares/tratamento farmacológico
Fármacos Neuroprotetores/farmacologia
Sepse/tratamento farmacológico
Receptor Nicotínico de Acetilcolina alfa7/genética
[Mh] Termos MeSH secundário: Animais
Citocinas/genética
Citocinas/metabolismo
Doenças Desmielinizantes/genética
Doenças Desmielinizantes/metabolismo
Doenças Desmielinizantes/patologia
Modelos Animais de Doenças
Regulação da Expressão Gênica
Fatores de Troca do Nucleotídeo Guanina/genética
Fatores de Troca do Nucleotídeo Guanina/metabolismo
Masculino
Proteína Quinase 1 Ativada por Mitógeno/genética
Proteína Quinase 1 Ativada por Mitógeno/metabolismo
Proteína Quinase 3 Ativada por Mitógeno/genética
Proteína Quinase 3 Ativada por Mitógeno/metabolismo
Doenças Musculares/genética
Doenças Musculares/metabolismo
Doenças Musculares/patologia
Neuregulina-1/genética
Neuregulina-1/metabolismo
Junção Neuromuscular/efeitos dos fármacos
Junção Neuromuscular/metabolismo
Junção Neuromuscular/patologia
Isoformas de Proteínas/antagonistas & inibidores
Isoformas de Proteínas/genética
Isoformas de Proteínas/metabolismo
Ratos
Ratos Sprague-Dawley
Nervo Isquiático/efeitos dos fármacos
Nervo Isquiático/metabolismo
Nervo Isquiático/patologia
Sepse/genética
Sepse/metabolismo
Sepse/patologia
Transdução de Sinais
Receptor Nicotínico de Acetilcolina alfa7/antagonistas & inibidores
Receptor Nicotínico de Acetilcolina alfa7/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Cytokines); 0 (Glial Cell Line-Derived Neurotrophic Factor); 0 (Guanine Nucleotide Exchange Factors); 0 (Neuregulin-1); 0 (Neuroprotective Agents); 0 (Nrg1 protein, rat); 0 (Protein Isoforms); 0 (alpha7 Nicotinic Acetylcholine Receptor); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
[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:180109
[St] Status:MEDLINE


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[PMID]:25815565
[Au] Autor:Saligan LN; Lukkahatai N; Holder G; Walitt B; Machado-Vieira R
[Ad] Endereço:a National Institute of Nursing Research, National Institutes of Health , Bethesda , MD , USA.
[Ti] Título:Lower brain-derived neurotrophic factor levels associated with worsening fatigue in prostate cancer patients during repeated stress from radiation therapy.
[So] Source:World J Biol Psychiatry;17(8):608-614, 2016 12.
[Is] ISSN:1814-1412
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Fatigue during cancer treatment is associated with depression. Neurotrophic factors play a major role in depression and stress and might provide insight into mechanisms of fatigue. This study investigated the association between plasma concentrations of three neurotrophic factors (BDNF, brain-derived neurotrophic factor; GDNF, glial-derived neurotrophic factor; and SNAPIN, soluble N-ethylmaleimide sensitive fusion attachment receptor-associated protein) and initial fatigue intensification during external beam radiation therapy (EBRT) in euthymic non-metastatic prostate cancer men. METHODS: Fatigue, as measured by the 13-item Functional Assessment of Cancer Therapy-Fatigue (FACT-F), and plasma neurotrophic factors were collected at baseline (prior to EBRT) and mid-EBRT. Subjects were categorized into fatigue and no fatigue groups using a > 3-point change in FACT-F scores between the two time points. Multiple linear regressions analysed the associations between fatigue and neurotrophic factors. RESULTS: FACT-F scores of 47 subjects decreased from baseline (43.95 ± 1.3) to mid-EBRT (38.36 ± 1.5, P < 0.001), indicating worsening fatigue. SNAPIN levels were associated with fatigue scores (r = 0.43, P = 0.005) at baseline. A significant decrease of BDNF concentration (P = 0.008) was found in fatigued subjects during EBRT (n = 39). CONCLUSIONS: Baseline SNAPIN and decreasing BDNF levels may influence worsening fatigue during EBRT. Further investigations are warranted to confirm their role in the pathophysiology and therapeutics of fatigue.
[Mh] Termos MeSH primário: Fator Neurotrófico Derivado do Encéfalo/sangue
Fadiga/etiologia
Neoplasias da Próstata/sangue
Neoplasias da Próstata/radioterapia
Radioterapia/efeitos adversos
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Depressão/etiologia
Fator Neurotrófico Derivado de Linhagem de Célula Glial/sangue
Seres Humanos
Modelos Lineares
Masculino
Meia-Idade
Índice de Gravidade de Doença
Estados Unidos
Proteínas de Transporte Vesicular/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., INTRAMURAL
[Nm] Nome de substância:
0 (Brain-Derived Neurotrophic Factor); 0 (GDNF protein, human); 0 (Glial Cell Line-Derived Neurotrophic Factor); 0 (SNAPIN protein, human); 0 (Vesicular Transport Proteins); 0 (brain-derived neurotrophic factor, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180123
[Lr] Data última revisão:
180123
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150328
[St] Status:MEDLINE


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[PMID]:28910445
[Au] Autor:Di G; Qi X; Zhao X; Zhang S; Danielson P; Zhou Q
[Ad] Endereço:Shandong Provincial Key Laboratory of Ophthalmology, Shandong Eye Institute, Shandong Academy of Medical Sciences, Qingdao, China.
[Ti] Título:Corneal Epithelium-Derived Neurotrophic Factors Promote Nerve Regeneration.
[So] Source:Invest Ophthalmol Vis Sci;58(11):4695-4702, 2017 Sep 01.
[Is] ISSN:1552-5783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose: To explore the neurotrophic factor expression in corneal epithelium and evaluate their effects on the trigeminal ganglion (TG) neurite outgrowth and corneal nerve regeneration in mice. Methods: The expression of neurotrophic factors was compared among the intact, regenerating, and regenerated mouse corneal epithelium. Mouse primary TG neurons were treated with the conditioned medium of mouse corneal epithelial cells. Nerve growth factor (NGF) neutralizing antibody and glial cell-derived neurotrophic factor (GDNF) neutralizing antibody were used to evaluate their roles in mouse corneal nerve regeneration and TG neurite outgrowth. The promoting effects of NGF and GDNF for the corneal nerve regeneration were further evaluated in the diabetic mice. Results: The expression of NGF and GDNF showed significant up-regulation in regenerating corneal epithelium and return to the preinjury levels in the regenerated epithelium, which was consistent with the progress of corneal subbasal nerve regeneration. The conditioned medium of corneal epithelial cells promoted the TG neurite outgrowth with extended branching and elongation. Furthermore, the blockage of either NGF or GDNF significantly impaired the promotion of the neurite outgrowth by the conditioned medium or the corneal nerve regeneration in normal mice. Moreover, the expression of NGF and GDNF was attenuated in the diabetic regenerating corneal epithelium as compared to that in normal mice, while exogenous NGF or GDNF supplement promoted the corneal epithelial and nerve regeneration in diabetic mice. Conclusions: Corneal epithelium expresses multiple neurotrophic factors, among which NGF and GDNF may play an important role in the corneal nerve regeneration.
[Mh] Termos MeSH primário: Córnea/inervação
Diabetes Mellitus Experimental/metabolismo
Epitélio Anterior/metabolismo
Fator Neurotrófico Derivado de Linhagem de Célula Glial/metabolismo
Fator de Crescimento Neural/metabolismo
Regeneração Nervosa/fisiologia
Nervo Trigêmeo/fisiologia
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Diabetes Mellitus Experimental/genética
Ensaio de Imunoadsorção Enzimática
Técnica Indireta de Fluorescência para Anticorpo
Fator Neurotrófico Derivado de Linhagem de Célula Glial/genética
Camundongos
Camundongos Endogâmicos C57BL
Fator de Crescimento Neural/genética
Neuritos/fisiologia
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Cicatrização/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Gdnf protein, mouse); 0 (Glial Cell Line-Derived Neurotrophic Factor); 9061-61-4 (Nerve Growth Factor)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170915
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.16-21372


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[PMID]:28797567
[Au] Autor:Zhang L; Zhu Z; Tan Z; Luo H; Hu X; Li Y
[Ad] Endereço:Tianjin Institute of Integrative Medicines for Acute Abdominal Diseases, Tianjin Nankai Hospital, Tianjin, China. Electronic address: lanqiuzhang@126.com.
[Ti] Título:Docosahexaenoic acid induces glial cell-line derived neurotrophic factor release in C6 glioma cells: Implications of antidepressant effects for docosahexaenoic acid.
[So] Source:Biochem Biophys Res Commun;491(4):1112-1117, 2017 Sep 30.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Dietary deficiency of n-3 polyunsaturated fatty acids (PUFAs) is involved in the pathophysiology and etiology of major depressive disorder. Supplementation with docosahexaenoic acid (DHA) exerts antidepressant-like effect; however, the molecular mechanism of DHA action remains unclear. Here we examined the effects of DHA on the modulation of glial cell line-derived neurotrophic factor (GDNF), which is essential for neural development, plasticity, neurogenesis, and survival. We demonstrated that DHA treatment significantly increased GDNF release in a concentration dependent manner in rat C6 glioma cells (C6 cells) and primary cultured rat astrocytes, which is also associated with increased expression of GDNF mRNA. Furthermore, the DHA-induced GDNF production was inhibited by mitogen activated protein kinase (MEK) inhibitor and protein kinase C (PKC) inhibitor, but not protein kinase A (PKA) inhibitor and p38 mitogen-activated protein kinase (MAPK) inhibitor. DHA-induced extracellular signal-regulated kinase (ERK) activation is dependent on the PKC, as demonstrated by its reversibility after pretreatment with PKC inhibitor. Moreover, fibroblast growth factor receptor (FGFR inhibitor) but not epidermal growth factor receptor (EGFR) inhibitor blocked the activation of ERK induced by DHA treatment. DHA-induced GDNF production was also blocked by FGFR inhibitor, suggesting that FGFR is also involved in ERK activation-mediated GDNF production induced by DHA. Our study demonstrates that DHA-induced release of GDNF, mediated by PKC and FGFR-dependent on ERK activation, may contribute to the antidepressant-like effect of DHA.
[Mh] Termos MeSH primário: Antidepressivos/farmacologia
Ácidos Docosa-Hexaenoicos/farmacologia
Fator Neurotrófico Derivado de Linhagem de Célula Glial/biossíntese
Glioma/metabolismo
[Mh] Termos MeSH secundário: Animais
Relação Dose-Resposta a Droga
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Fator Neurotrófico Derivado de Linhagem de Célula Glial/antagonistas & inibidores
Glioma/patologia
Ratos
Receptores de Fatores de Crescimento de Fibroblastos/metabolismo
Relação Estrutura-Atividade
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antidepressive Agents); 0 (Gdnf protein, mouse); 0 (Glial Cell Line-Derived Neurotrophic Factor); 0 (Receptors, Fibroblast Growth Factor); 25167-62-8 (Docosahexaenoic Acids); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170812
[St] Status:MEDLINE


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[PMID]:28753652
[Au] Autor:Schwenkgrub J; Zaremba M; Joniec-Maciejak I; Cudna A; Mirowska-Guzel D; Kurkowska-Jastrzebska I
[Ad] Endereço:Department of Experimental and Clinical Pharmacology, Centre for Preclinical Research and Technology (CePT), Medical University of Warsaw, Warsaw, Poland.
[Ti] Título:The phosphodiesterase inhibitor, ibudilast, attenuates neuroinflammation in the MPTP model of Parkinson's disease.
[So] Source:PLoS One;12(7):e0182019, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Since the degeneration of the nigrostriatal dopaminergic pathway in Parkinson's disease (PD) is associated with the inflammation process and decreased levels of cyclic nucleotides, inhibition of up-regulated cyclic nucleotide phosphodiesterases (PDEs) appears to be a promising therapeutic strategy. We used ibudilast (IBD), a non-selective PDE3,4,10,11 inhibitor, due to the abundant PDE 4 and 10 expression in the striatum. The present study for the first time examined the efficacy of IBD in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD. METHODS: IBD [0, 20, 30, 40, or 50 mg/kg] was injected b.i.d. subcutaneously for nine days to three-month-old male C57Bl/10Tar mice, beginning two days prior to MPTP (60 mg/kg) intoxication. High-pressure liquid chromatography, Western blot analysis, and real time RT-PCR methods were applied. RESULTS: Our study demonstrated that chronic administration of IBD attenuated astroglial reactivity and increased glial cell-derived neurotrophic factor (GDNF) production in the striatum. Moreover, IBD reduced TNF-α, IL-6, and IL-1ß expression. CONCLUSION: IBD had a well-defined effect on astroglial activation in the mouse model of PD; however, there was no protective effect in the acute phase of injury. Diminished inflammation and an increased level of GDNF may provide a better outcome in the later stages of neurodegeneration.
[Mh] Termos MeSH primário: Astrócitos/efeitos dos fármacos
Intoxicação por MPTP/tratamento farmacológico
Intoxicação por MPTP/metabolismo
Doença de Parkinson/tratamento farmacológico
Piridinas/farmacologia
Piridinas/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Astrócitos/metabolismo
Modelos Animais de Doenças
Fator Neurotrófico Derivado de Linhagem de Célula Glial/metabolismo
Interleucina-1beta/metabolismo
Interleucina-6/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Fármacos Neuroprotetores/farmacologia
Fármacos Neuroprotetores/uso terapêutico
Doença de Parkinson/etiologia
Doença de Parkinson/metabolismo
Inibidores de Fosfodiesterase/farmacologia
Inibidores de Fosfodiesterase/uso terapêutico
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glial Cell Line-Derived Neurotrophic Factor); 0 (Interleukin-1beta); 0 (Interleukin-6); 0 (Neuroprotective Agents); 0 (Phosphodiesterase Inhibitors); 0 (Pyridines); 0 (Tumor Necrosis Factor-alpha); M0TTH61XC5 (ibudilast)
[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:170729
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0182019


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[PMID]:28506996
[Au] Autor:Park HJ; Bolton EC
[Ad] Endereço:Department of Molecular and Integrative Physiology, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA.
[Ti] Título:RET-mediated glial cell line-derived neurotrophic factor signaling inhibits mouse prostate development.
[So] Source:Development;144(12):2282-2293, 2017 06 15.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In humans and rodents, the prostate gland develops from the embryonic urogenital sinus (UGS). The androgen receptor (AR) is thought to control the expression of morphogenetic genes in inductive UGS mesenchyme, which promotes proliferation and cytodifferentiation of the prostatic epithelium. However, the nature of the AR-regulated morphogenetic genes and the mechanisms whereby AR controls prostate development are not understood. Glial cell line-derived neurotrophic factor (GDNF) binds GDNF family receptor α1 (GFRα1) and signals through activation of RET tyrosine kinase. Gene disruption studies in mice have revealed essential roles for GDNF signaling in development; however, its role in prostate development is unexplored. Here, we establish novel roles of GDNF signaling in mouse prostate development. Using an organ culture system for prostate development and mutant mice, we demonstrate that RET-mediated GDNF signaling in UGS increases proliferation of mesenchyme cells and suppresses androgen-induced proliferation and differentiation of prostate epithelial cells, inhibiting prostate development. We also identify as a GDNF-repressed gene and and as androgen-repressed genes in UGS, thus establishing reciprocal regulatory crosstalk between AR and GDNF signaling in prostate development.
[Mh] Termos MeSH primário: Fator Neurotrófico Derivado de Linhagem de Célula Glial/metabolismo
Próstata/embriologia
Próstata/metabolismo
Proteínas Proto-Oncogênicas c-ret/metabolismo
[Mh] Termos MeSH secundário: Actinas/metabolismo
Animais
Diferenciação Celular
Proliferação Celular
Di-Hidrotestosterona/farmacologia
Feminino
Fator Neurotrófico Derivado de Linhagem de Célula Glial/genética
Receptores de Fator Neurotrófico Derivado de Linhagem de Célula Glial/genética
Receptores de Fator Neurotrófico Derivado de Linhagem de Célula Glial/metabolismo
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Mutantes
Camundongos Transgênicos
Morfogênese/genética
Morfogênese/fisiologia
Técnicas de Cultura de Órgãos
Gravidez
Próstata/citologia
Proteínas Proto-Oncogênicas c-ret/genética
Receptor Cross-Talk
Receptores Androgênicos/efeitos dos fármacos
Receptores Androgênicos/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (AR protein, mouse); 0 (Actins); 0 (Gdnf protein, mouse); 0 (Gfra1 protein, mouse); 0 (Glial Cell Line-Derived Neurotrophic Factor); 0 (Glial Cell Line-Derived Neurotrophic Factor Receptors); 0 (Receptors, Androgen); 08J2K08A3Y (Dihydrotestosterone); EC 2.7.10.1 (Proto-Oncogene Proteins c-ret); EC 2.7.10.1 (Ret protein, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171126
[Lr] Data última revisão:
171126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170517
[St] Status:MEDLINE
[do] DOI:10.1242/dev.145086


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[PMID]:28490528
[Au] Autor:Geraci S; Chacon-Caldera J; Cullen-McEwen L; Schad LR; Sticht C; Puelles VG; Bertram JF; Gretz N
[Ad] Endereço:Medical Research Centre, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany.
[Ti] Título:Combining new tools to assess renal function and morphology: a holistic approach to study the effects of aging and a congenital nephron deficit.
[So] Source:Am J Physiol Renal Physiol;313(3):F576-F584, 2017 Sep 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Recently, new methods for assessing renal function in conscious mice (transcutaneous assessment) and for counting and sizing all glomeruli in whole kidneys (MRI) have been described. In the present study, these methods were used to assess renal structure and function in aging mice, and in mice born with a congenital low-nephron endowment. Age-related nephron loss was analyzed in adult C57BL/6 mice (10-50 wk of age), and congenital nephron deficit was assessed in glial cell line-derived neurotrophic factor heterozygous (GDNF HET)-null mutant mice. Renal function was measured through the transcutaneous quantitation of fluorescein isothiocyanate-sinistrin half-life ( ) in conscious mice. MRI was used to image, count, and size cationic-ferritin labeled glomeruli in whole kidneys ex vivo. Design-based stereology was used to validate the MRI measurements of glomerular number and mean volume. In adult C57BL/6 mice, older age was associated with fewer and larger glomeruli, and a rightward shift in the glomerular size distribution. These changes coincided with a decrease in renal function. GNDF HET mice had a congenital nephron deficit that was associated with glomerular hypertrophy and exacerbated by aging. These findings suggest that glomerular hypertrophy and hyperfiltration are compensatory processes that can occur in conjunction with both age-related nephron loss and congenital nephron deficiency. The combination of measurement of renal function in conscious animals and quantitation of glomerular number, volume, and volume distribution provides a powerful new tool for investigating aspects of renal aging and functional changes.
[Mh] Termos MeSH primário: Envelhecimento/patologia
Fator Neurotrófico Derivado de Linhagem de Célula Glial/deficiência
Nefropatias/patologia
Nefropatias/fisiopatologia
Testes de Função Renal
Glomérulos Renais/patologia
Imagem por Ressonância Magnética
Néfrons/anormalidades
[Mh] Termos MeSH secundário: Fatores Etários
Animais
Modelos Animais de Doenças
Fluoresceínas/administração & dosagem
Fluoresceínas/farmacocinética
Corantes Fluorescentes/administração & dosagem
Corantes Fluorescentes/farmacocinética
Predisposição Genética para Doença
Fator Neurotrófico Derivado de Linhagem de Célula Glial/genética
Taxa de Filtração Glomerular
Meia-Vida
Heterozigoto
Hipertrofia
Nefropatias/congênito
Glomérulos Renais/fisiopatologia
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Oligossacarídeos/administração & dosagem
Oligossacarídeos/farmacocinética
Fenótipo
Valor Preditivo dos Testes
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fluoresceins); 0 (Fluorescent Dyes); 0 (Gdnf protein, mouse); 0 (Glial Cell Line-Derived Neurotrophic Factor); 0 (Oligosaccharides); 0 (fluorescein-isothiocyanate sinistrin)
[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:170512
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00329.2015


  9 / 3056 MEDLINE  
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[PMID]:28489907
[Au] Autor:Luo L; Kim SW; Lee HK; Kim ID; Lee H; Lee JK
[Ad] Endereço:Department of Anatomy, Inha University School of Medicine, Inchon, Korea.
[Ti] Título:Anti-oxidative effects of 4-hydroxybenzyl alcohol in astrocytes confer protective effects in autocrine and paracrine manners.
[So] Source:PLoS One;12(5):e0177322, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:4-Hydroxybenzyl alcohol (4-HBA) is an important phenolic constituent of Gastrodia elata Blume (GEB), a traditional herbal medicine used in East Asia. Many activities have been reported to underlie the beneficial effects of 4-HBA in the brain, and in particular, its anti-inflammatory, anti-oxidative, and anti-zinc-toxic effects have been implicated in the postischemic brain. Here, the authors investigated the anti-oxidative effect of 4-HBA on astrocytes and sought to identify the underlying molecular mechanisms involved. 4-HBA dose-dependently suppressed H2O2-induced astrocyte cell death. More specifically, pre-incubation of C6 cells (an astrocyte cell line) with 100 µM 4-HBA for 6 hrs increased survival when cells were treated with H2O2 (100 µM, 1 hr) from 54.2±0.7% to 85.9±1.5%. In addition, 4-HBA was found to up-regulate and activate Nrf2, and subsequently, to induce the expressions of several anti-oxidative genes, such as, HO-1, NQO1, and GCLM. Notably, HO-1 was induced by 3.4-fold in 4-HBA-treated C6 cells, and siRNA-mediated HO-1 knockdown demonstrated that Nrf2 activation and HO-1 induction were responsible for the observed cytoprotective effect of 4-HBA. ERK and Akt signaling pathways were activated by 4-HBA in C6 cells, suggesting their involvements in protective effect of 4-HBA. In addition, 4-HBA-conditioned astrocyte culture medium was found to have neuroprotective effects on primary neuronal cultures or fresh C6 cells exposed to oxidative stress, and these effects seemed to be mediated by glial cell line-derived neurotrophic factor (GDNF) and vascular endothelial growth factor (VEGF), which both accumulated in 4-HBA-treated astrocyte culture media. Thus, the 4-HBA-mediated activation of Nrf2 and induction of HO-1 in astrocytes were found to act via autocrine and paracrine mechanisms to confer protective effects. Furthermore, given the pleiotropic effects of 4-HBA with respect to its targeting of various brain cell types and functions, it would appear that 4-HBA has therapeutic potential for the prevention and amelioration of various brain diseases.
[Mh] Termos MeSH primário: Antioxidantes/farmacologia
Astrócitos/efeitos dos fármacos
Álcoois Benzílicos/farmacologia
Morte Celular/efeitos dos fármacos
Fármacos Neuroprotetores/farmacologia
Estresse Oxidativo/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Antioxidantes/química
Astrócitos/citologia
Astrócitos/metabolismo
Álcoois Benzílicos/química
Células Cultivadas
Feminino
Gastrodia/química
Fator Neurotrófico Derivado de Linhagem de Célula Glial/metabolismo
Heme Oxigenase-1/metabolismo
Peróxido de Hidrogênio/metabolismo
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Camundongos
Camundongos Endogâmicos ICR
Fator 2 Relacionado a NF-E2/metabolismo
Fármacos Neuroprotetores/química
Proteínas Proto-Oncogênicas c-akt/metabolismo
Regulação para Cima/efeitos dos fármacos
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Benzyl Alcohols); 0 (Glial Cell Line-Derived Neurotrophic Factor); 0 (NF-E2-Related Factor 2); 0 (Neuroprotective Agents); 0 (Vascular Endothelial Growth Factor A); 1A3AH1FP1B (4-hydroxybenzyl alcohol); BBX060AN9V (Hydrogen Peroxide); EC 1.14.14.18 (Heme Oxygenase-1); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170908
[Lr] Data última revisão:
170908
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170511
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0177322


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[PMID]:28481001
[Au] Autor:Ee X; Yan Y; Hunter DA; Schellhardt L; Sakiyama-Elbert SE; Mackinnon SE; Wood MD
[Ad] Endereço:Division of Plastic and Reconstructive Surgery, Department of Surgery, Washington University School of Medicine, Campus Box 8238, 660 South Euclid Avenue, St. Louis, Missouri, 63110.
[Ti] Título:Transgenic SCs expressing GDNF-IRES-DsRed impair nerve regeneration within acellular nerve allografts.
[So] Source:Biotechnol Bioeng;114(9):2121-2130, 2017 Sep.
[Is] ISSN:1097-0290
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Providing temporally regulated glial cell line-derived neurotrophic factor (GDNF) to injured nerve can promote robust axon regeneration. However, it is poorly understood why providing highly elevated levels of GDNF to nerve can lead to axon entrapment in the zone containing elevated GDNF. This limited understanding represents an obstacle to the translation of GDNF therapies to treat nerve injuries clinically. Here, we investigated how transgenic Schwann cells (SCs) overexpressing GDNF-IRES-DsRed impact nerve regeneration. Cultured primary SCs were transduced with lentiviruses (GDNF-overexpressing transgenic SCs), one of which provides the capability to express high levels of GDNF and regulate temporal GDNF expression. These SC groups were transplanted into acellular nerve allografts (ANAs) bridging a 14 mm rat sciatic nerve defect. GDNF-overexpressing transgenic SCs expressing GDNF for as little as 1 week decreased axon regeneration across ANAs and caused extensive extracellular matrix (ECM) remodeling. To determine whether additional gene expression changes beyond GDNF transgene expression occurred in GDNF-overexpressing transgenic SCs, microarray analysis of GDNF-overexpressing transgenic SCs compared to untreated SCs was performed. Microarray analysis revealed a set of common genes regulated in transgenic SC groups expressing high levels of GDNF compared to untreated SCs. A co-culture model of GDNF-overexpressing transgenic SCs with fibroblasts (FBs) revealed differential FB ECM-related gene expression compared to untreated SCs. These data suggest a component of axon entrapment is independent of GDNF's impact on axons. Biotechnol. Bioeng. 2017;114: 2121-2130. © 2017 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Fator Neurotrófico Derivado de Linhagem de Célula Glial/metabolismo
Proteínas Luminescentes/metabolismo
Regeneração Nervosa/fisiologia
Traumatismos dos Nervos Periféricos/fisiopatologia
Traumatismos dos Nervos Periféricos/terapia
Nervo Isquiático/lesões
Nervo Isquiático/transplante
[Mh] Termos MeSH secundário: Aloenxertos
Animais
Sistema Livre de Células
Células Cultivadas
Regeneração Tecidual Guiada/métodos
Sítios Internos de Entrada Ribossomal/fisiologia
Masculino
Ratos
Ratos Endogâmicos Lew
Células de Schwann/fisiologia
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glial Cell Line-Derived Neurotrophic Factor); 0 (Internal Ribosome Entry Sites); 0 (Luminescent Proteins); 0 (fluorescent protein 583)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170509
[St] Status:MEDLINE
[do] DOI:10.1002/bit.26335



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