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[PMID]:28460633
[Au] Autor:Zhang Z; Zheng W; Xie H; Chai R; Wang J; Zhang H; He S
[Ad] Endereço:Allergy and Clinical Immunology Research Centre, The First Affiliated Hospital of Jinzhou Medical University, No. 2, Section 5, Renmin Street, Guta District, Jinzhou, 121001, Liaoning, People's Republic of China.
[Ti] Título:Up-regulated expression of substance P in CD8 T cells and NK1R on monocytes of atopic dermatitis.
[So] Source:J Transl Med;15(1):93, 2017 May 01.
[Is] ISSN:1479-5876
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Large numbers of CD8 T cells were observed in atopic dermatitis (AD) skin, and monocytes from AD patients showed increased prostaglandin E2 production. However, little is known about the expression of substance P (SP) and its receptor NK1R in blood leukocytes of patients with AD. OBJECTIVE: To explore the expression of SP and NK1R in leukocytes of AD and the influence of allergens on SP and NK1R expression. METHODS: The expression levels of SP and NK1R in patients with AD were examined by flow cytometry, ELISA and a mouse AD model. RESULTS: The plasma SP level was 4.9-fold higher in patients with AD than in HC subjects. Both the percentage of SP expression in the population and mean fluorescence intensity (MFI) of SP expression were elevated in CD8 T cells in the blood of AD patients. However, both the CD14 NK1R population and MFI of NK1R expression on CD14 cells were enhanced in the blood of AD patients. Allergens ASWE, HDME and PPE failed to up-regulate SP expression in CD8 T cells. However, allergens ASWE and HDME both enhanced NK1R expression on CD14 blood leukocytes regardless of AD or HC subjects. OVA-sensitized AD mice showed an elevated proportion and MFI of SP-expressing CD8 T cells in the blood, which agrees with the SP expression situation in human AD blood. Injection of SP into mouse skin did not up-regulate NK1R expression on monocytes. CONCLUSIONS: An elevated plasma SP level, up-regulated expression of SP and NK1R indicate that the SP/NK1R complex is important in the development of AD. Therefore, SP and NK1R antagonist or blocker agents may help to treat patients with AD. Trial registration Registration number: ChiCTR-BOC-16010279; Registration date: Dec., 28, 2016; retrospectively registered.
[Mh] Termos MeSH primário: Linfócitos T CD8-Positivos/imunologia
Dermatite Atópica/genética
Dermatite Atópica/imunologia
Monócitos/patologia
Receptores da Neurocinina-1/metabolismo
Substância P/genética
Regulação para Cima/genética
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Alérgenos/imunologia
Animais
Estudos de Casos e Controles
Dermatite Atópica/sangue
Citometria de Fluxo
Seres Humanos
Camundongos Endogâmicos BALB C
Meia-Idade
Ovalbumina/imunologia
Substância P/sangue
Substância P/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Allergens); 0 (Receptors, Neurokinin-1); 33507-63-0 (Substance P); 9006-59-1 (Ovalbumin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1186/s12967-017-1196-6


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[PMID]:29061788
[Au] Autor:Pohl A; Kappler R; Mühling J; VON Schweinitz D; Berger M
[Ad] Endereço:Department of Pediatric Surgery, Dr von Hauner Children's Hospital, University Hospital, Ludwig-Maximilians-University Munich, Munich, Germany.
[Ti] Título:Expression of Truncated Neurokinin-1 Receptor in Childhood Neuroblastoma is Independent of Tumor Biology and Stage.
[So] Source:Anticancer Res;37(11):6079-6085, 2017 11.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Neuroblastoma is an embryonal malignancy arising from the aberrant growth of neural crest progenitor cells of the sympathetic nervous system. The tachykinin receptor 1 (TACR1) - substance P complex is associated with tumoral angiogenesis and cell proliferation in a variety of cancer types. Inhibition of TACR1 was recently described to impede growth of NB cell lines. However, the relevance of TACR1 in clinical settings is unknown. PATIENTS AND METHODS: We investigated gene expression levels of full-length and truncated TACR1 in 59 neuroblastomas and correlated these data with the patients' clinical parameters such as outcome, metastasis, International Neuroblastoma Staging System (INSS) status, MYCN proto-oncogene, bHLH transcription factor (MYCN) status, gender and age. RESULTS: Our results indicated that TACR1 is ubiquitously expressed in neuroblastoma but expression levels are independent of clinical parameters. CONCLUSION: Our data suggest that TACR1 might serve as a potent anticancer target in a large variety of patients with neuroblastoma, independent of tumor biology and clinical stage.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/metabolismo
Regulação Neoplásica da Expressão Gênica
Neuroblastoma/metabolismo
Receptores da Neurocinina-1/metabolismo
[Mh] Termos MeSH secundário: Adolescente
Adulto
Biomarcadores Tumorais/genética
Criança
Pré-Escolar
Feminino
Seguimentos
Seres Humanos
Lactente
Recém-Nascido
Metástase Linfática
Masculino
Proteína Proto-Oncogênica N-Myc/genética
Proteína Proto-Oncogênica N-Myc/metabolismo
Estadiamento de Neoplasias
Neuroblastoma/patologia
Prognóstico
Receptores da Neurocinina-1/genética
Taxa de Sobrevida
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (MYCN protein, human); 0 (N-Myc Proto-Oncogene Protein); 0 (Receptors, Neurokinin-1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171025
[St] Status:MEDLINE


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[PMID]:29061769
[Au] Autor:Berger M; VON Schweinitz D
[Ad] Endereço:Department of Pediatric Surgery, Research Laboratories, Dr. von Hauner Children's Hospital, Ludwig-Maximilians-University, Munich, Germany michael.fabian.berger@gmail.com.
[Ti] Título:Therapeutic Innovations for Targeting Childhood Neuroblastoma: Implications of the Neurokinin-1 Receptor System.
[So] Source:Anticancer Res;37(11):5911-5918, 2017 11.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Neuroblastoma is the most common solid extracranial malignant tumor in children. Despite recent advances in the treatment of this heterogenous tumor with surgery and chemotherapy, the prognosis in advanced stages remains poor. Interestingly, neuroblastoma is one of the few solid tumors, to date, in which an effect for targeted immunotherapy has been proven in controlled clinical trials, giving hope for further advances in the treatment of this and other tumors by targeted therapy. A large array of novel therapeutic options for targeted therapy of neuroblastoma is on the horizon. To this repεrtoirε, the neurokinin-1 receptor (NK1R) system was recently added. The present article explores the most recent developments in targeting neuroblastoma cells via the NK1R and how this new knowledge could be helpful to create new anticancer therapies agains neuroblastoma and other cancers.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Imunoterapia
Terapia de Alvo Molecular
Neuroblastoma/terapia
Receptores da Neurocinina-1/química
[Mh] Termos MeSH secundário: Criança
Seres Humanos
Neuroblastoma/imunologia
Receptores da Neurocinina-1/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Receptors, Neurokinin-1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171025
[St] Status:MEDLINE


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[PMID]:28931039
[Au] Autor:Bright FM; Vink R; Byard RW; Duncan JR; Krous HF; Paterson DS
[Ad] Endereço:Discipline of Anatomy and Pathology, Adelaide Medical School, University of Adelaide, Adelaide, SA, Australia.
[Ti] Título:Abnormalities in substance P neurokinin-1 receptor binding in key brainstem nuclei in sudden infant death syndrome related to prematurity and sex.
[So] Source:PLoS One;12(9):e0184958, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sudden infant death syndrome (SIDS) involves failure of arousal to potentially life threatening events, including hypoxia, during sleep. While neuronal dysfunction and abnormalities in neurotransmitter systems within the medulla oblongata have been implicated, the specific pathways associated with autonomic and cardiorespiratory failure are unknown. The neuropeptide substance P (SP) and its tachykinin neurokinin-1 receptor (NK1R) have been shown to play an integral role in the modulation of homeostatic function in the medulla, including regulation of respiratory rhythm generation, integration of cardiovascular control, and modulation of the baroreceptor reflex and mediation of the chemoreceptor reflex in response to hypoxia. Abnormalities in SP neurotransmission may therefore result in autonomic dysfunction during sleep and contribute to SIDS deaths. [125I] Bolton Hunter SP autoradiography was used to map the distribution and density of the SP, NK1R to 13 specific nuclei intimately related to cardiorespiratory function and autonomic control in the human infant medulla of 55 SIDS and 21 control (non-SIDS) infants. Compared to controls, SIDS cases exhibited a differential, abnormal developmental profile of the SP/NK1R system in the medulla. Furthermore the study revealed significantly decreased NK1R binding within key medullary nuclei in SIDS cases, principally in the nucleus tractus solitarii (NTS) and all three subdivisions of the inferior portion of the olivo-cerebellar complex; the principal inferior olivary complex (PIO), medial accessory olive (MAO) and dorsal accessory olive (DAO). Altered NK1R binding was significantly influenced by prematurity and male sex, which may explain the increased risk of SIDS in premature and male infants. Abnormal NK1R binding in these medullary nuclei may contribute to the defective interaction of critical medullary mechanisms with cerebellar sites, resulting in an inability of a SIDS infant to illicit appropriate respiratory and motor responses to life threatening challenges during sleep. These observations support the concept that abnormalities in a multi-neurotransmitter network within key nuclei of the medullary homeostatic system may underlie the pathogenesis of a subset of SIDS cases.
[Mh] Termos MeSH primário: Tronco Encefálico/patologia
Recém-Nascido Prematuro/metabolismo
Bulbo/patologia
Núcleo Olivar/patologia
Receptores da Neurocinina-1/metabolismo
Substância P/metabolismo
Morte Súbita do Lactente/patologia
[Mh] Termos MeSH secundário: Tronco Encefálico/metabolismo
Estudos de Coortes
Feminino
Seres Humanos
Lactente
Recém-Nascido
Masculino
Bulbo/metabolismo
Núcleo Olivar/metabolismo
Ligação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Neurokinin-1); 33507-63-0 (Substance P)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170921
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184958


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[PMID]:28827386
[Au] Autor:Suvas S
[Ad] Endereço:Department of Ophthalmology/Kresge Eye Institute, Wayne State University School of Medicine, Detroit, MI 48201; ssuvas@med.wayne.edu.
[Ti] Título:Role of Substance P Neuropeptide in Inflammation, Wound Healing, and Tissue Homeostasis.
[So] Source:J Immunol;199(5):1543-1552, 2017 Sep 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Substance P (SP) is an undecapeptide present in the CNS and the peripheral nervous system. SP released from the peripheral nerves exerts its biological and immunological activity via high-affinity neurokinin 1 receptor (NK1R). SP is also produced by immune cells and acts as an autocrine or paracrine fashion to regulate the function of immune cells. In addition to its proinflammatory role, SP and its metabolites in combination with insulin-like growth factor-1 are shown to promote the corneal epithelial wound healing. Recently, we showed an altered ocular surface homeostasis in unmanipulated NK1R mice, suggesting the role of SP-NK1R signaling in ocular surface homeostasis under steady-state. This review summarizes the immunobiology of SP and its effect on immune cells and immunity to microbial infection. In addition, the effect of SP in inflammation, wound healing, and corneal epithelial homeostasis in the eye is discussed.
[Mh] Termos MeSH primário: Inflamação/imunologia
Sistema Nervoso
Neuroimunomodulação
Neurotransmissores/imunologia
Substância P/imunologia
[Mh] Termos MeSH secundário: Animais
Córnea/metabolismo
Córnea/patologia
Homeostase
Seres Humanos
Fator de Crescimento Insulin-Like I/análogos & derivados
Fator de Crescimento Insulin-Like I/metabolismo
Camundongos
Receptores da Neurocinina-1/genética
Receptores da Neurocinina-1/metabolismo
Transdução de Sinais
Cicatrização
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Neurotransmitter Agents); 0 (Receptors, Neurokinin-1); 0 (insulin-like growth factor-1 D peptide); 33507-63-0 (Substance P); 67763-96-6 (Insulin-Like Growth Factor I)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171028
[Lr] Data última revisão:
171028
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170823
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601751


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[PMID]:28710964
[Au] Autor:Recio R; Vengut-Climent E; Mouillac B; Orcel H; López-Lázaro M; Calderón-Montaño JM; Álvarez E; Khiar N; Fernández I
[Ad] Endereço:Departamento de Química Orgánica y Farmacéutica, Facultad de Farmacia, Universidad de Sevilla, 41012 Sevilla, Spain.
[Ti] Título:Design, synthesis and biological studies of a library of NK1-Receptor Ligands Based on a 5-arylthiosubstituted 2-amino-4,6-diaryl-3-cyano-4H-pyran core: Switch from antagonist to agonist effect by chemical modification.
[So] Source:Eur J Med Chem;138:644-660, 2017 Sep 29.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:A library of 5-arylthiosubstituted 2-amino-4,6-diaryl-3-cyano-4H-pyrans has been synthesized as a new family of non-peptide NK1 receptor ligands by a one-pot cascade process. Their biological effects via interaction with the NK1 receptor were experimentally determined as percentage of inhibition (for antagonists) and percentage of activation (for agonists), compared to the substance P (SP) effect, in IPone assay. A set of these amino compounds was found to inhibit the action of SP, and therefore can be considered as a new family of SP-antagonists. Interestingly, the acylation of the 2-amino position causes a switch from antagonist to agonist activity. The 5-phenylsulfonyl-2-amino derivative 17 showed the highest antagonist activity, while the 5-p-tolylsulfenyl-2-trifluoroacetamide derivative 20R showed the highest agonist effect. As expected, in the case of the 5-sulfinylderivatives, there was an enantiomeric discrimination in favor of one of the two enantiomers, specifically those with (S ,R ) configuration. The anticancer activity studies assessed by using human A-549 lung cancer cells and MRC-5 non-malignant lung fibroblasts, revealed a statistically significant selective cytotoxic effect of some of these 2-amino-4H-pyran derivatives toward the lung cancer cells. These studies demonstrated that the newly synthesized 4H-pyran derivatives can be used as a starting point for the synthesis of novel SP-antagonists with higher anticancer activity in the future.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Desenho de Drogas
Antagonistas do Receptor de Neuroquinina-1/farmacologia
Piranos/farmacologia
Receptores da Neurocinina-1/agonistas
Receptores da Neurocinina-1/metabolismo
[Mh] Termos MeSH secundário: Antineoplásicos/síntese química
Antineoplásicos/química
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Ensaios de Seleção de Medicamentos Antitumorais
Seres Humanos
Ligantes
Estrutura Molecular
Antagonistas do Receptor de Neuroquinina-1/síntese química
Antagonistas do Receptor de Neuroquinina-1/química
Piranos/síntese química
Piranos/química
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Ligands); 0 (Neurokinin-1 Receptor Antagonists); 0 (Pyrans); 0 (Receptors, Neurokinin-1)
[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:170716
[St] Status:MEDLINE


  7 / 3220 MEDLINE  
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[PMID]:28647476
[Au] Autor:Peng L; Jia X; Zhao J; Cui R; Yan M
[Ad] Endereço:Department of Hepatology and Gastroenterology, Qilu Hospital of Shandong University, Jinan, Shandong Province 250012, PR China; Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06510, USA.
[Ti] Título:Substance P promotes hepatic stellate cell proliferation and activation via the TGF-ß1/Smad-3 signaling pathway.
[So] Source:Toxicol Appl Pharmacol;329:293-300, 2017 Aug 15.
[Is] ISSN:1096-0333
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Prolonged activation and proliferation of hepatic stellate cells (HSCs) usually results in the initiation and progression of liver fibrosis following injury. Recent studies have shown that Substance P (SP) participates in the development of fibrosis. However, whether SP is involved in liver fibrosis, especially in the activation and proliferation of HSCs, is largely unknown. In the present study, we measured the effects of a series of concentrations of SP on the cell viability and activation of HSC-T6 cells and LX2 cells. The underlying mechanism was also investigated. We found that SP effectively increased cell viability, both in an MTT assay (p<0.05) and in a lactate dehydrogenase activity assay (LDH) (p<0.05). Moreover, SP upregulated the protein expression of α-SMA and Collagen I (both p<0.05) and decreased the release of lipid droplets (LDs) (p<0.05), all of which are associated with HSC activation. Apoptosis analysis revealed that SP can attenuate the increase of cell apoptosis induced by serum withdrawal (p<0.05). Furthermore, these effects were all blocked by an SP receptor antagonist, L732138. More importantly, L732138 decreased the activation of the TGF-ß1/Smad3 signaling pathway, which is highly associated with liver fibrosis. Taken together, our results demonstrate that SP can promote HSC proliferation and induce HSC activation via the TGF-ß1/Smad3 signaling pathway.
[Mh] Termos MeSH primário: Proliferação Celular/efeitos dos fármacos
Células Estreladas do Fígado/efeitos dos fármacos
Cirrose Hepática/induzido quimicamente
Transdução de Sinais/efeitos dos fármacos
Proteína Smad3/metabolismo
Substância P/toxicidade
Fator de Crescimento Transformador beta1/metabolismo
[Mh] Termos MeSH secundário: Actinas/metabolismo
Animais
Apoptose/efeitos dos fármacos
Colágeno Tipo I/metabolismo
Relação Dose-Resposta a Droga
Células Estreladas do Fígado/enzimologia
Células Estreladas do Fígado/patologia
Seres Humanos
Gotículas Lipídicas/efeitos dos fármacos
Gotículas Lipídicas/metabolismo
Cirrose Hepática/enzimologia
Cirrose Hepática/patologia
Antagonistas do Receptor de Neuroquinina-1/farmacologia
Ratos
Receptores da Neurocinina-1/efeitos dos fármacos
Receptores da Neurocinina-1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ACTA2 protein, human); 0 (Acta2 protein, rat); 0 (Actins); 0 (Collagen Type I); 0 (Madh3 protein, rat); 0 (Neurokinin-1 Receptor Antagonists); 0 (Receptors, Neurokinin-1); 0 (SMAD3 protein, human); 0 (Smad3 Protein); 0 (TGFB1 protein, human); 0 (Tgfb1 protein, rat); 0 (Transforming Growth Factor beta1); 33507-63-0 (Substance P)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170731
[Lr] Data última revisão:
170731
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170626
[St] Status:MEDLINE


  8 / 3220 MEDLINE  
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[PMID]:28366470
[Au] Autor:Saito H; Katagiri A; Okada S; Mikuzuki L; Kubo A; Suzuki T; Ohara K; Lee J; Gionhaku N; Iinuma T; Bereiter DA; Iwata K
[Ad] Endereço:Department of Complete Denture Prosthodontics, Nihon University School of Dentistry, 1-8-13 Kandasurugadai, Chiyoda-ku, Tokyo 101-8310, Japan; Department of Physiology, Nihon University School of Dentistry, 1-8-13 Kandasurugadai, Chiyoda-ku, Tokyo 101-8310, Japan. Electronic address: dehi14017@g.nih
[Ti] Título:Ascending projections of nociceptive neurons from trigeminal subnucleus caudalis: A population approach.
[So] Source:Exp Neurol;293:124-136, 2017 Jul.
[Is] ISSN:1090-2430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Second-order neurons in trigeminal subnucleus caudalis (Vc) and upper cervical spinal cord (C1) are critical for craniofacial pain processing and project rostrally to terminate in: ventral posteromedial thalamic nucleus (VPM), medial thalamic nuclei (MTN) and parabrachial nuclei (PBN). The contribution of each region to trigeminal nociception was assessed by the number of phosphorylated extracellular signal-regulated kinase-immunoreactive (pERK-IR) neurons co-labeled with fluorogold (FG). The phenotype of pERK-IR neurons was further defined by the expression of neurokinin 1 receptor (NK1). The retrograde tracer FG was injected into VPM, MTN or PBN of the right hemisphere and after seven days, capsaicin was injected into the left upper lip in male rats. Nearly all pERK-IR neurons were found in superficial laminae of Vc-C1 ipsilateral to the capsaicin injection. Nearly all VPM and MTN FG-labeled neurons in Vc-C1 were found contralateral to the injection site, whereas FG-labeled neurons were found bilaterally after PBN injection. The percentage of FG-pERK-NK1-IR neurons was significantly greater (>10%) for PBN projection neurons than for VPM and MTN projection neurons (<3%). pERK-NK1-IR VPM projection neurons were found mainly in the middle-Vc, while pERK-NK1-immunoreactive MTN or PBN projection neurons were found in the middle-Vc and caudal Vc-C1. These results suggest that a significant percentage of capsaicin-responsive neurons in superficial laminae of Vc-C1 project directly to PBN, while neurons that project to VPM and MTN are subject to greater modulation by pERK-IR local interneurons. Furthermore, the rostrocaudal distribution differences of FG-pERK-NK1-IR neurons in Vc-C1 may reflect functional differences between these projection areas regarding craniofacial pain.
[Mh] Termos MeSH primário: Dor Facial/patologia
Nociceptores/patologia
Núcleos do Trigêmeo/patologia
[Mh] Termos MeSH secundário: Animais
Capsaicina/toxicidade
Modelos Animais de Doenças
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Dor Facial/induzido quimicamente
Masculino
Núcleo Mediodorsal do Tálamo/patologia
Vias Neurais/patologia
Vias Neurais/fisiologia
Nociceptores/metabolismo
Núcleos Parabraquiais/patologia
Ratos
Ratos Sprague-Dawley
Receptores da Neurocinina-1/metabolismo
Fármacos do Sistema Sensorial/toxicidade
Estatísticas não Paramétricas
Estilbamidinas/metabolismo
Núcleos Ventrais do Tálamo/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-hydroxy-4,4'-diamidinostilbene, methanesulfonate salt); 0 (Receptors, Neurokinin-1); 0 (Sensory System Agents); 0 (Stilbamidines); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); S07O44R1ZM (Capsaicin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170404
[St] Status:MEDLINE


  9 / 3220 MEDLINE  
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[PMID]:28341744
[Au] Autor:Zhang YX; Li XF; Yuan GQ; Hu H; Song XY; Li JY; Miao XK; Zhou TX; Yang WL; Zhang XW; Mou LY; Wang R
[Ad] Endereço:From the Institute of Biochemistry and Molecular Biology, School of Life Sciences and Key Laboratory of Preclinical Study for New Drugs of Gansu Province, School of Basic Medical Sciences, Lanzhou University, Lanzhou 730000, China and.
[Ti] Título:ß-Arrestin 1 has an essential role in neurokinin-1 receptor-mediated glioblastoma cell proliferation and G /M phase transition.
[So] Source:J Biol Chem;292(21):8933-8947, 2017 May 26.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Glioblastoma is the most common malignant brain tumor and has a poor prognosis. Tachykinin receptor neurokinin-1 (NK1R) is a promising target in glioblastoma therapy because of its overexpression in human glioblastoma. NK1R agonists promote glioblastoma cell growth, whereas NK1R antagonists efficiently inhibit cell growth both and However, the molecular mechanisms involved in these effects are incompletely understood. ß-Arrestins (ARRBs) serve as scaffold proteins and adapters to mediate intracellular signal transduction. Here we show that the ARRB1-mediated signaling pathway is essential for NK1-mediated glioblastoma cell proliferation. ARRB1 knockdown significantly inhibited NK1-mediated glioblastoma cell proliferation and induced G /M phase cell cycle arrest. ARRB1 knockdown cells showed remarkable down-regulation of CDC25C/CDK1/cyclin B1 activity. We also demonstrated that ARRB1 mediated prolonged phosphorylation of ERK1/2 and Akt in glioblastoma cells induced by NK1R activation. ERK1/2 and Akt phosphorylation are involved in regulating CDC25C/CDK1/cyclin B1 activity. The lack of long-term ERK1/2 and Akt activation in ARRB1 knockdown cells was at least partly responsible for the delayed cell cycle progression and proliferation. Moreover, we found that ARRB1-mediated ERK1/2 and Akt phosphorylation regulated the transcriptional activity of both NF-κB and AP-1, which were involved in cyclin B1 expression. ARRB1 deficiency increased the sensitivity of glioblastoma cells to the treatment of NK1R antagonists. Taken together, our results suggest that ARRB1 plays an essential role in NK1R-mediated cell proliferation and G /M transition in glioblastoma cells. Interference with ARRB1-mediated signaling via NK1R may have potential significance for therapeutic strategies targeting glioblastoma.
[Mh] Termos MeSH primário: Fase G2
Glioblastoma/metabolismo
Sistema de Sinalização das MAP Quinases
Receptores da Neurocinina-1/metabolismo
beta-Arrestina 1/metabolismo
[Mh] Termos MeSH secundário: Proteína Quinase CDC2
Linhagem Celular
Ciclina B1/genética
Ciclina B1/metabolismo
Quinases Ciclina-Dependentes/genética
Quinases Ciclina-Dependentes/metabolismo
Técnicas de Silenciamento de Genes
Glioblastoma/genética
Glioblastoma/terapia
Seres Humanos
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
Proteínas Proto-Oncogênicas c-akt/genética
Proteínas Proto-Oncogênicas c-akt/metabolismo
Receptores da Neurocinina-1/genética
beta-Arrestina 1/genética
Fosfatases cdc25/genética
Fosfatases cdc25/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ARRB1 protein, human); 0 (CCNB1 protein, human); 0 (Cyclin B1); 0 (Receptors, Neurokinin-1); 0 (beta-Arrestin 1); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 2.7.11.22 (CDC2 Protein Kinase); EC 2.7.11.22 (CDK1 protein, human); EC 2.7.11.22 (Cyclin-Dependent Kinases); EC 2.7.11.24 (MAPK1 protein, human); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3); EC 3.1.3.48 (CDC25C protein, human); EC 3.1.3.48 (cdc25 Phosphatases)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170326
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M116.770420


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[PMID]:28301610
[Au] Autor:Fong G; Backman LJ; Alfredson H; Scott A; Danielson P
[Ad] Endereço:Dept. of Integrative Medical Biology, Anatomy, Umeå University, Umeå, Sweden.
[Ti] Título:The effects of substance P and acetylcholine on human tenocyte proliferation converge mechanistically via TGF-ß1.
[So] Source:PLoS One;12(3):e0174101, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Previous in vitro studies on human tendon cells (tenocytes) have demonstrated that the exogenous administration of substance P (SP) and acetylcholine (ACh) independently result in tenocyte proliferation, which is a prominent feature of tendinosis. Interestingly, the possible link between SP and ACh has not yet been explored in human tenocytes. Recent studies in other cell types demonstrate that both SP and ACh independently upregulate TGF-ß1 expression via their respective receptors, the neurokinin 1 receptor (NK-1R) and muscarinic ACh receptors (mAChRs). Furthermore, TGF-ß1 has been shown to downregulate NK-1R expression in human keratocytes. The aim of this study was to examine if TGF-ß1 is the intermediary player involved in mediating the proliferative pathway shared by SP and ACh in human tenocytes. The results showed that exogenous administration of SP and ACh both caused significant upregulation of TGF-ß1 at the mRNA and protein levels. Exposing cells to TGF-ß1 resulted in increased cell viability of tenocytes, which was blocked in the presence of the TGFßRI/II kinase inhibitor. In addition, the proliferative effects of SP and ACh on tenocytes were reduced by the TGFßRI/II kinase inhibitor; this supports the hypothesis that the proliferative effects of these signal substances are mediated via the TGF-ß axis. Furthermore, exogenous TGF-ß1 downregulated NK-1R and mAChRs expression at both the mRNA and protein levels, and these effects were negated by simultaneous exposure to the TGFßRI/II kinase inhibitor, suggesting a negative feedback loop. In conclusion, the results indicate that TGF-ß1 is the intermediary player through which the proliferative actions of both SP and ACh converge mechanistically.
[Mh] Termos MeSH primário: Acetilcolina/farmacologia
Proliferação Celular/efeitos dos fármacos
Substância P/farmacologia
Tenócitos/efeitos dos fármacos
Fator de Crescimento Transformador beta1/fisiologia
[Mh] Termos MeSH secundário: Células Cultivadas
Seres Humanos
Receptores Muscarínicos/metabolismo
Receptores da Neurocinina-1/metabolismo
Tenócitos/citologia
Tenócitos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Muscarinic); 0 (Receptors, Neurokinin-1); 0 (Transforming Growth Factor beta1); 33507-63-0 (Substance P); N9YNS0M02X (Acetylcholine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170317
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0174101



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