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[PMID]:28957681
[Au] Autor:Clements MP; Byrne E; Camarillo Guerrero LF; Cattin AL; Zakka L; Ashraf A; Burden JJ; Khadayate S; Lloyd AC; Marguerat S; Parrinello S
[Ad] Endereço:Cell Interactions and Cancer Group, MRC London Institute of Medical Sciences, Du Cane Road, London W12 0NN, United Kingdom; Institute of Clinical Sciences, Faculty of Medicine, Imperial College London, Du Cane Road, London W12 0NN, United Kingdom.
[Ti] Título:The Wound Microenvironment Reprograms Schwann Cells to Invasive Mesenchymal-like Cells to Drive Peripheral Nerve Regeneration.
[So] Source:Neuron;96(1):98-114.e7, 2017 Sep 27.
[Is] ISSN:1097-4199
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Schwann cell dedifferentiation from a myelinating to a progenitor-like cell underlies the remarkable ability of peripheral nerves to regenerate following injury. However, the molecular identity of the differentiated and dedifferentiated states in vivo has been elusive. Here, we profiled Schwann cells acutely purified from intact nerves and from the wound and distal regions of severed nerves. Our analysis reveals novel facets of the dedifferentiation response, including acquisition of mesenchymal traits and a Myc module. Furthermore, wound and distal dedifferentiated Schwann cells constitute different populations, with wound cells displaying increased mesenchymal character induced by localized TGFß signaling. TGFß promotes invasion and crosstalks with Eph signaling via N-cadherin to drive collective migration of the Schwann cells across the wound. Consistently, Tgfbr2 deletion in Schwann cells resulted in misdirected and delayed reinnervation. Thus, the wound microenvironment is a key determinant of Schwann cell identity, and it promotes nerve repair through integration of multiple concerted signals. VIDEO ABSTRACT.
[Mh] Termos MeSH primário: Diferenciação Celular
Microambiente Celular/fisiologia
Células Mesenquimais Estromais/citologia
Células Mesenquimais Estromais/fisiologia
Regeneração Nervosa/fisiologia
Traumatismos dos Nervos Periféricos/fisiopatologia
Células de Schwann/citologia
Células de Schwann/fisiologia
[Mh] Termos MeSH secundário: Animais
Caderinas/fisiologia
Movimento Celular/fisiologia
Células Cultivadas
Feminino
Masculino
Camundongos
Camundongos Transgênicos
Traumatismos dos Nervos Periféricos/patologia
Cultura Primária de Células
Ratos
Ratos Transgênicos
Receptores da Família Eph/fisiologia
Nervo Isquiático/lesões
Nervo Isquiático/fisiologia
Fator de Crescimento Transformador beta/genética
Fator de Crescimento Transformador beta/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cadherins); 0 (Transforming Growth Factor beta); EC 2.7.10.1 (Receptors, Eph Family)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170929
[St] Status:MEDLINE


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[PMID]:28826721
[Au] Autor:Chen J; Li L; Yang Z; Luo J; Yeh S; Chang C
[Ad] Endereço:Sex Hormone Research Center, Department of Urology, The First Affiliated Hospital, Xi'an Jiaotong University, Xi'an, 710061, China; George Whipple Lab for Cancer Research, Departments of Pathology and Urology, The Wilmot Cancer Center, University of Rochester Medical Center, Rochester, NY, 14642, US
[Ti] Título:Androgen-deprivation therapy with enzalutamide enhances prostate cancer metastasis via decreasing the EPHB6 suppressor expression.
[So] Source:Cancer Lett;408:155-163, 2017 Nov 01.
[Is] ISSN:1872-7980
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Early studies suggested that using ADT with the recently developed anti-androgen Enzalutamide (Enz, also named as MDV3100 could extent castration resistant prostate cancer (CRPC) patients' survival an extra 4.8 months. Yet the therapy in most patients might eventually fail due to development of Enz-resistance. Here we found Enz might also increase some unwanted side-effects via increasing the CRPC cell invasion that might involve altering the Enz-mediated androgen receptor (AR)/EPHB6 suppressor/JNK signaling. Results from multiple clinical surveys also indicated that EPHP6 might function as a suppressor of PCa metastasis. Mechanism dissection revealed that Enz-mediated AR might function via binding to the androgen-response-element (ARE) on the EPHB6 promoter to decrease EPHB6 suppressor expression, which might then activate the phosphorylation of JNK signals to increase the CRPC cell invasion. Targeting this newly identified AR/EPHB6/JNK signaling with JNK inhibitor (SP600125) may then block/reverse the Enz-increased CRPC cell invasion. Collectively, our results suggest that Enz may increase CRPC cell invasion via altering the AR/EPHB6/JNK/MMP9 signaling and targeting this newly identified signaling may help us to increase the Enz efficacy to better suppress the CRPC at the later metastatic stage.
[Mh] Termos MeSH primário: Antagonistas de Androgênios/farmacologia
Feniltioidantoína/análogos & derivados
Neoplasias de Próstata Resistentes à Castração/secundário
Receptores da Família Eph/metabolismo
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Resistência a Medicamentos Antineoplásicos
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Masculino
Invasividade Neoplásica
Metástase Neoplásica
Feniltioidantoína/farmacologia
Neoplasias de Próstata Resistentes à Castração/tratamento farmacológico
Neoplasias de Próstata Resistentes à Castração/metabolismo
Receptores Androgênicos/química
Receptores Androgênicos/metabolismo
Receptores da Família Eph/genética
Transdução de Sinais
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Androgen Antagonists); 0 (MDV 3100); 0 (Receptors, Androgen); 2010-15-3 (Phenylthiohydantoin); EC 2.7.10.1 (EPHB6 protein, human); EC 2.7.10.1 (Receptors, Eph Family)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170823
[St] Status:MEDLINE


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[PMID]:28751189
[Au] Autor:Charmsaz S; Scott AM; Boyd AW
[Ad] Endereço:Leukaemia Foundation Laboratory, QIMR-Berghofer Medical Research Institute, Brisbane, Australia; Department of Medicine, University of Queensland, Brisbane, Australia; Department of Surgery, Royal College of Surgeons, Dublin, Ireland. Electronic address: saracharmsaz@rcsi.ie.
[Ti] Título:Targeted therapies in hematological malignancies using therapeutic monoclonal antibodies against Eph family receptors.
[So] Source:Exp Hematol;54:31-39, 2017 Oct.
[Is] ISSN:1873-2399
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The use of monoclonal antibodies (mAbs) and molecules derived from them has achieved considerable attention and success in recent years, establishing this mode of therapy as an important therapeutic strategy in many cancers, in particular hematological tumors. mAbs recognize cell surface antigens expressed on target cells and mediate their function through various mechanisms such as antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, or immune system modulation. The efficacy of mAb therapy can be improved when they are conjugated to a highly potent payloads, including cytotoxic drugs and radiolabeled isotopes. The Eph family of proteins has received considerable attention in recent years as therapeutic targets for treatment of both solid and hematological cancers. High expression of Eph receptors on cancer cells compared with low expression levels in normal adult tissues makes them an attractive candidate for cancer immunotherapy. In this review, we detail the modes of action of antibody-based therapies with a focus on the Eph family of proteins as potential targets for therapy in hematological malignancies.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/uso terapêutico
Regulação Neoplásica da Expressão Gênica
Neoplasias Hematológicas/tratamento farmacológico
Terapia de Alvo Molecular
Proteínas de Neoplasias/antagonistas & inibidores
Receptores da Família Eph/antagonistas & inibidores
[Mh] Termos MeSH secundário: Anticorpos Monoclonais/biossíntese
Citotoxicidade Celular Dependente de Anticorpos/efeitos dos fármacos
Antineoplásicos/uso terapêutico
Ativação do Complemento/efeitos dos fármacos
Citotoxinas/química
Citotoxinas/uso terapêutico
Neoplasias Hematológicas/genética
Neoplasias Hematológicas/imunologia
Neoplasias Hematológicas/patologia
Seres Humanos
Imunoconjugados/química
Imunoconjugados/uso terapêutico
Imunomodulação/efeitos dos fármacos
Imunoterapia/métodos
Proteínas de Neoplasias/genética
Proteínas de Neoplasias/imunologia
Receptores da Família Eph/genética
Receptores da Família Eph/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Antineoplastic Agents); 0 (Cytotoxins); 0 (Immunoconjugates); 0 (Neoplasm Proteins); EC 2.7.10.1 (Receptors, Eph Family)
[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:170729
[St] Status:MEDLINE


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[PMID]:28589441
[Au] Autor:Tosato G
[Ad] Endereço:Laboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Building 37, Room 4124, Bethesda, MD, 20892, USA. tosatog@mail.nih.gov.
[Ti] Título:Ephrin ligands and Eph receptors contribution to hematopoiesis.
[So] Source:Cell Mol Life Sci;74(18):3377-3394, 2017 Sep.
[Is] ISSN:1420-9071
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Hematopoietic stem and progenitor cells reside predominantly in the bone marrow. They supply billions of mature blood cells every day during life through maturation into multilineage progenitors and self-renewal. Newly produced mature cells serve to replenish the pool of circulating blood cells at the end of their life-span. These mature blood cells and a few hematopoietic progenitors normally exit the bone marrow through the sinusoidal vessels, a specialized venous vascular system that spreads throughout the bone marrow. Many signals regulate the coordinated mobilization of hematopoietic cells from the bone marrow to the circulation. In this review, we present recent advances on hematopoiesis and hematopoietic cell mobilization with a focus on the role of Ephrin ligands and their Eph receptors. These constitute a large family of transmembrane ligands and receptors that play critical roles in development and postnatally. New insights point to distinct roles of ephrin and Eph in different aspects of hematopoiesis.
[Mh] Termos MeSH primário: Efrinas/metabolismo
Hematopoese/fisiologia
Ligantes
Receptores da Família Eph/metabolismo
[Mh] Termos MeSH secundário: Animais
Medula Óssea/metabolismo
Diferenciação Celular
Células-Tronco Hematopoéticas/citologia
Células-Tronco Hematopoéticas/metabolismo
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Ephrins); 0 (Ligands); EC 2.7.10.1 (Receptors, Eph Family)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170830
[Lr] Data última revisão:
170830
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170608
[St] Status:MEDLINE
[do] DOI:10.1007/s00018-017-2566-1


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[PMID]:28535565
[Au] Autor:Yu LN; Sun LH; Wang M; Wang LJ; Wu Y; Yu J; Wang WN; Zhang FJ; Li X; Yan M
[Ad] Endereço:Department of Anesthesiology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
[Ti] Título:EphrinB-EphB Signaling Induces Hyperalgesia through ERK5/CREB Pathway in Rats.
[So] Source:Pain Physician;20(4):E563-E574, 2017 May.
[Is] ISSN:2150-1149
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: There are numerous studies implicating that EphB receptors and ephrinB ligands play important roles in modulating the transduction of spinal nociceptive information. EphrinB-EphB signaling may contribute to hyperalgesia via various kinds of downstream molecules, the mechanisms of which have not been completely understood. OBJECTIVE: The aim of the present study was to identify whether ephrinB-EphB signaling could contribute to hyperalgesia through ERK5/CREB pathway. STUDY DESIGN: Controlled animal study. SETTING: University laboratory. METHODS: This study attempted to detect the changes of pain behaviors and the protein level of p-ERK5 and p-CREB by activating EphB receptors in the spinal cord of rats. To further confirm our hypothesis, we designed LV-siRNA for knockdown of spinal ERK5. When ERK5 was inhibited, we recorded the changes of spinal p-CREB expression and the pain behaviors of rats after activating EphB receptors. We also confirmed this conclusion in rat CCI model. Statistical analyses were performed using GraphPad Prism 5. RESULTS: Intrathecal injection of ephrinB2-Fc in rats evoked thermal hyperalgesia and mechanical allodynia, along with activation of ERK5 and CREB in the spinal cord. Knockdown of ERK5 inhibited ephrinB2-Fc-induced CREB activation and hyperalgesia. Blocking EphB receptors prevented CCI-induced neuropathic pain and spinal ERK5/CREB activation. LIMITATIONS: More underlying mechanisms that underlie the relationship between ephrinB-EphB signaling and ERK5/CREB pathway will need to be explored in future studies. CONCLUSIONS: Our study suggests that ERK5/CREB pathway plays important roles in the transduction of nociceptive information associated with ephrinB-EphB signaling. This study provides further understanding of the downstream mechanisms of ephrinB-EphB signaling and helps to explore new targets for treating pathological pain.
[Mh] Termos MeSH primário: Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico/metabolismo
Efrina-B2/metabolismo
Hiperalgesia/metabolismo
Proteína Quinase 7 Ativada por Mitógeno/metabolismo
Receptores da Família Eph/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Astrócitos/metabolismo
Hiperalgesia/fisiopatologia
Masculino
Microglia/metabolismo
Neuralgia/fisiopatologia
Neurônios/metabolismo
Medição da Dor
Ratos
Ratos Sprague-Dawley
Medula Espinal/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclic AMP Response Element-Binding Protein); 0 (Ephrin-B2); EC 2.7.10.1 (Receptors, Eph Family); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 7)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170717
[Lr] Data última revisão:
170717
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170524
[St] Status:MEDLINE


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[PMID]:28434841
[Au] Autor:Nagaraja S; Vitanza NA; Woo PJ; Taylor KR; Liu F; Zhang L; Li M; Meng W; Ponnuswami A; Sun W; Ma J; Hulleman E; Swigut T; Wysocka J; Tang Y; Monje M
[Ad] Endereço:Department of Neurology, Stanford University, Palo Alto, CA 94305, USA.
[Ti] Título:Transcriptional Dependencies in Diffuse Intrinsic Pontine Glioma.
[So] Source:Cancer Cell;31(5):635-652.e6, 2017 May 08.
[Is] ISSN:1878-3686
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Diffuse intrinsic pontine glioma (DIPG) is a fatal pediatric cancer with limited therapeutic options. The majority of cases of DIPG exhibit a mutation in histone-3 (H3K27M) that results in oncogenic transcriptional aberrancies. We show here that DIPG is vulnerable to transcriptional disruption using bromodomain inhibition or CDK7 blockade. Targeting oncogenic transcription through either of these methods synergizes with HDAC inhibition, and DIPG cells resistant to HDAC inhibitor therapy retain sensitivity to CDK7 blockade. Identification of super-enhancers in DIPG provides insights toward the cell of origin, highlighting oligodendroglial lineage genes, and reveals unexpected mechanisms mediating tumor viability and invasion, including potassium channel function and EPH receptor signaling. The findings presented demonstrate transcriptional vulnerabilities and elucidate previously unknown mechanisms of DIPG pathobiology.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia
Azepinas/farmacologia
Neoplasias do Tronco Encefálico/tratamento farmacológico
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Glioma/tratamento farmacológico
Inibidores de Histona Desacetilases/farmacologia
Ácidos Hidroxâmicos/farmacologia
Indóis/farmacologia
Fenilenodiaminas/farmacologia
Inibidores de Proteínas Quinases/farmacologia
Pirimidinas/farmacologia
Transcrição Genética/efeitos dos fármacos
Triazóis/farmacologia
[Mh] Termos MeSH secundário: Animais
Neoplasias do Tronco Encefálico/genética
Neoplasias do Tronco Encefálico/metabolismo
Neoplasias do Tronco Encefálico/patologia
Proliferação Celular/efeitos dos fármacos
Montagem e Desmontagem da Cromatina/efeitos dos fármacos
Quinases Ciclina-Dependentes/antagonistas & inibidores
Quinases Ciclina-Dependentes/genética
Quinases Ciclina-Dependentes/metabolismo
Relação Dose-Resposta a Droga
Resistência a Medicamentos Antineoplásicos
Sinergismo Farmacológico
Feminino
Glioma/genética
Glioma/metabolismo
Glioma/patologia
Histonas/genética
Histonas/metabolismo
Seres Humanos
Masculino
Camundongos Endogâmicos NOD
Camundongos SCID
Mutação
Proteínas Nucleares/antagonistas & inibidores
Proteínas Nucleares/genética
Proteínas Nucleares/metabolismo
Cultura Primária de Células
Interferência de RNA
Receptores da Família Eph/genética
Receptores da Família Eph/metabolismo
Transdução de Sinais/efeitos dos fármacos
Fatores de Tempo
Fatores de Transcrição/antagonistas & inibidores
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
Transfecção
Células Tumorais Cultivadas
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 ((+)-JQ1 compound); 0 (Azepines); 0 (BRD4 protein, human); 0 (Histone Deacetylase Inhibitors); 0 (Histones); 0 (Hydroxamic Acids); 0 (Indoles); 0 (Nuclear Proteins); 0 (Phenylenediamines); 0 (Protein Kinase Inhibitors); 0 (Pyrimidines); 0 (THZ1 compound); 0 (Transcription Factors); 0 (Triazoles); 9647FM7Y3Z (panobinostat); EC 2.7.10.1 (Receptors, Eph Family); EC 2.7.11.22 (Cyclin-Dependent Kinases); EC 2.7.11.22 (cyclin-dependent kinase-activating kinase)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170919
[Lr] Data última revisão:
170919
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170425
[St] Status:MEDLINE


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[PMID]:28322822
[Au] Autor:Ventrella R; Kaplan N; Getsios S
[Ad] Endereço:Department of Dermatology, Northwestern University, 303 E. Chicago Ave, Chicago, IL 60611, USA.
[Ti] Título:Asymmetry at cell-cell interfaces direct cell sorting, boundary formation, and tissue morphogenesis.
[So] Source:Exp Cell Res;358(1):58-64, 2017 Sep 01.
[Is] ISSN:1090-2422
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:During development, cells of seemingly homogenous character sort themselves out into distinct compartments in order to generate cell types with specialized features that support tissue morphogenesis and function. This process is often driven by receptors at the cell membrane that probe the extracellular microenvironment for specific ligands and alter downstream signaling pathways impacting transcription, cytoskeletal organization, and cell adhesion to regulate cell sorting and subsequent boundary formation. This review will focus on two of these receptor families, Eph and Notch, both of which are intrinsically non-adhesive and are activated by a unique set of ligands that are asymmetrically distributed from their receptor on neighboring cells. Understanding the requirement of asymmetric ligand-receptor signaling at the membrane under homeostatic conditions gives insight into how misregulation of these pathways contributes to boundary disruption in diseases like cancer.
[Mh] Termos MeSH primário: Adesão Celular/fisiologia
Diferenciação Celular/fisiologia
Efrinas/metabolismo
Morfogênese/fisiologia
Receptores da Família Eph/metabolismo
Transdução de Sinais/fisiologia
[Mh] Termos MeSH secundário: Animais
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Ephrins); EC 2.7.10.1 (Receptors, Eph Family)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171005
[Lr] Data última revisão:
171005
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170322
[St] Status:MEDLINE


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[PMID]:28248712
[Au] Autor:Zhou X; Zhang C; Zhang C; Peng Y; Wang Y; Xu H
[Ad] Endereço:From the Department of Anesthesiology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China (X.Z.); Department of Gastroenterology, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu, China (Chenjing Z.); Department of Digestive Endoscopy, Chuzhou Hospital of Integrated Traditional Chinese Medicine and Western Medicine, Chuzhou, China (Congjuan Z.); Department of Anesthesiology, Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing, Jiangsu, China (Y.P.); Department of Anesthesiology, Taizhou People's Hospital, Taizhou, Jiangsu, China (Y.W.); and Department of Anesthesiology, the First People's Hospital of Shanghai Transportation University, Shanghai, China (H.X.).
[Ti] Título:MicroRNA-182-5p Regulates Nerve Injury-induced Nociceptive Hypersensitivity by Targeting Ephrin Type-b Receptor 1.
[So] Source:Anesthesiology;126(5):967-977, 2017 May.
[Is] ISSN:1528-1175
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The authors and others have previously shown that the up-regulation of spinal ephrin type-b receptor 1 plays an essential role in the pathologic process of nerve injury-induced nociceptive hypersensitivity, but the regulatory mechanism remains unclear. METHODS: Radiant heat and von Frey filaments were applied to assess nociceptive behaviors. Real-time quantitative polymerase chain reaction, Western blotting, fluorescence in situ hybridization, immunofluorescence, immunohistochemistry, dual-luciferase reporter gene assays, recombinant lentivirus, and small interfering RNA were used to characterize the likely mechanisms. RESULTS: Periphery nerve injury induced by chronic constriction injury of the sciatic nerve significantly reduced spinal microRNA-182-5p (miR-182-5p) expression levels, which were inversely correlated with spinal ephrin type-b receptor 1 expression (R = 0.90; P < 0.05; n = 8). The overexpression of miR-182-5p in the spinal cord prevented and reversed the nociceptive behaviors induced by sciatic nerve injury, accompanied by a decreased expression of spinal ephrin type-b receptor 1 (recombinant lentiviruses containing pre-microRNA-182: 1.91 ± 0.34 vs. 1.24 ± 0.31, n = 4; miR-182-5p mimic: 2.90 ± 0.48 vs. 1.51 ± 0.25, n = 4). In contrast, the down-regulation of spinal miR-182-5p facilitated the nociceptive behaviors induced by sciatic nerve injury and increased the expression of spinal ephrin type-b receptor 1 (1.0 ± 0.26 vs. 1.74 ± 0.31, n = 4). Moreover, the down-regulation of miR-182-5p and up-regulation of ephrin type-b receptor 1 caused by sciatic nerve injury were mediated by the N-methyl-D-aspartate receptor. CONCLUSIONS: Collectively, our findings reveal that the spinal ephrin type-b receptor 1 is regulated by miR-182-5p in nerve injury-induced nociceptive hypersensitivity.
[Mh] Termos MeSH primário: MicroRNAs/metabolismo
Dor Nociceptiva/fisiopatologia
Receptores da Família Eph/metabolismo
Nervo Isquiático/fisiopatologia
Regulação para Cima/fisiologia
[Mh] Termos MeSH secundário: Animais
Western Blotting
Regulação para Baixo
Efrinas
Fluorescência
Imunofluorescência
Imuno-Histoquímica
Masculino
Camundongos
MicroRNAs/genética
Dor Nociceptiva/genética
Dor Nociceptiva/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Receptores da Família Eph/genética
Nervo Isquiático/metabolismo
Medula Espinal/metabolismo
Regulação para Cima/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ephrins); 0 (MicroRNAs); 0 (Mirn182 microRNA, mouse); EC 2.7.10.1 (Receptors, Eph Family)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170503
[Lr] Data última revisão:
170503
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170302
[St] Status:MEDLINE
[do] DOI:10.1097/ALN.0000000000001588


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[PMID]:28095646
[Au] Autor:Hwang YS; Daar IO
[Ad] Endereço:Cancer and Developmental Biology Laboratory, National Cancer Institute, Frederick, Maryland, 21702.
[Ti] Título:A frog's view of EphrinB signaling.
[So] Source:Genesis;55(1-2), 2017 Jan.
[Is] ISSN:1526-968X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cell-cell and cell-substrate adhesion are essential to the proper formation and maintenance of tissue patterns during development, and deregulation of these processes can lead to invasion and metastasis of cancer cells. Cell surface adhesion and signaling molecules are key players in both normal development and cancer progression. One set of cell surface proteins, the Eph receptor tyrosine kinases and their membrane-bound ligands, ephrins, are significant regulators of these processes. During embryonic development, the Eph/ephrin signaling system is involved in cell-cell contact events that result in cell sorting and boundary formation between receptor and ligand bearing cells. When migrating cells that display the membrane bound ligands or receptors come in contact with cells bearing the cognate partner, the response may be adhesion or repulsion, ultimately leading to the proper positioning of these cells. During cancer progression, the signaling between these receptor/ligand pairs is often deregulated, leading to increased invasion and metastasis. To gain mechanistic insight into the pathways that mediate Eph receptor and ephrin signaling we have relied upon a very tractable system, the frog Xenopus. This model system has proven to be extremely versatile, and represents a relatively quick and manipulable system to explore signaling events and the in vivo processes affected by these signals.
[Mh] Termos MeSH primário: Adesão Celular/genética
Desenvolvimento Embrionário/genética
Efrinas/genética
Receptores da Família Eph/genética
[Mh] Termos MeSH secundário: Animais
Efrinas/biossíntese
Regulação da Expressão Gênica no Desenvolvimento
Seres Humanos
Modelos Animais
Receptores da Família Eph/biossíntese
Transdução de Sinais/genética
Xenopus/genética
Xenopus/crescimento & desenvolvimento
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Ephrins); EC 2.7.10.1 (Receptors, Eph Family)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170523
[Lr] Data última revisão:
170523
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170118
[St] Status:MEDLINE
[do] DOI:10.1002/dvg.23002


  10 / 649 MEDLINE  
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[PMID]:27825440
[Au] Autor:Cayuso J; Dzementsei A; Fischer JC; Karemore G; Caviglia S; Bartholdson J; Wright GJ; Ober EA
[Ad] Endereço:Division of Developmental Biology, Mill Hill Laboratories, The Francis Crick Institute, London NW7 1AA, UK.
[Ti] Título:EphrinB1/EphB3b Coordinate Bidirectional Epithelial-Mesenchymal Interactions Controlling Liver Morphogenesis and Laterality.
[So] Source:Dev Cell;39(3):316-328, 2016 Nov 07.
[Is] ISSN:1878-1551
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Positioning organs in the body often requires the movement of multiple tissues, yet the molecular and cellular mechanisms coordinating such movements are largely unknown. Here, we show that bidirectional signaling between EphrinB1 and EphB3b coordinates the movements of the hepatic endoderm and adjacent lateral plate mesoderm (LPM), resulting in asymmetric positioning of the zebrafish liver. EphrinB1 in hepatoblasts regulates directional migration and mediates interactions with the LPM, where EphB3b controls polarity and movement of the LPM. EphB3b in the LPM concomitantly repels hepatoblasts to move leftward into the liver bud. Cellular protrusions controlled by Eph/Ephrin signaling mediate hepatoblast motility and long-distance cell-cell contacts with the LPM beyond immediate tissue interfaces. Mechanistically, intracellular EphrinB1 domains mediate EphB3b-independent hepatoblast extension formation, while EpB3b interactions cause their destabilization. We propose that bidirectional short- and long-distance cell interactions between epithelial and mesenchyme-like tissues coordinate liver bud formation and laterality via cell repulsion.
[Mh] Termos MeSH primário: Efrina-B1/metabolismo
Efrina-B3/metabolismo
Epitélio/embriologia
Lateralidade Funcional
Fígado/embriologia
Mesoderma/embriologia
Morfogênese
Receptores da Família Eph/metabolismo
Proteínas de Peixe-Zebra/metabolismo
[Mh] Termos MeSH secundário: Animais
Padronização Corporal
Movimento Celular
Forma Celular
Epitélio/metabolismo
Mesoderma/metabolismo
Pseudópodes/metabolismo
Peixe-Zebra/embriologia
Peixe-Zebra/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (EphB3b protein, zebrafish); 0 (Ephrin-B1); 0 (Ephrin-B3); 0 (Zebrafish Proteins); EC 2.7.10.1 (Receptors, Eph Family)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171014
[Lr] Data última revisão:
171014
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161110
[St] Status:MEDLINE



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