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[PMID]:28711627
[Au] Autor:Bednarska O; Walter SA; Casado-Bedmar M; Ström M; Salvo-Romero E; Vicario M; Mayer EA; Keita ÅV
[Ad] Endereço:Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden; Department of Gastroenterology, Linköping University, Linköping, Sweden.
[Ti] Título:Vasoactive Intestinal Polypeptide and Mast Cells Regulate Increased Passage of Colonic Bacteria in Patients With Irritable Bowel Syndrome.
[So] Source:Gastroenterology;153(4):948-960.e3, 2017 Oct.
[Is] ISSN:1528-0012
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND & AIMS: Irritable bowel syndrome (IBS) is associated with intestinal dysbiosis and symptoms of IBS develop following gastroenteritis. We aimed to study the passage of live bacteria through the colonic epithelium, and determine the role of mast cells (MCs) and vasoactive intestinal polypeptide (VIP) in barrier regulation in IBS and healthy individuals. METHODS: Colon biopsies from 32 women with IBS and 15 age-matched healthy women (controls) were mounted in Ussing chambers; we measured numbers of fluorescently labeled Escherichia coli HS and Salmonella typhimurium that passed through from the mucosal side to the serosal side of the tissue. Some biopsies were exposed to agents that block the VIP receptors (VPAC1 and VPAC2) or MCs. Levels of VIP and tryptase were measured in plasma and biopsy lysates. Number of MCs and MCs that express VIP or VIP receptors were quantified by immunofluorescence. Biopsies from an additional 5 patients with IBS and 4 controls were mounted in chambers and Salmonella were added; we studied passage routes through the epithelium by transmission electron microscopy and expression of tight junctions by confocal microscopy. RESULTS: In colon biopsies from patients with IBS, larger numbers of E coli HS and S typhimurium passed through the epithelium than in biopsies from controls (P < .0005). In transmission electron microscopy analyses, bacteria were found to cross the epithelium via only the transcellular route. Bacterial passage was reduced in biopsies from patients with IBS and controls after addition of antibodies against VPACs or ketotifen, which inhibits MCs. Plasma samples from patients with IBS had higher levels of VIP than plasma samples from controls. Biopsies from patients with IBS had higher levels of tryptase, larger numbers of MCs, and a higher percentage of MCs that express VPAC1 than biopsies from controls. In biopsies from patients with IBS, addition of Salmonella significantly reduced levels of occludin; subsequent addition of ketotifen significantly reversed this effect. CONCLUSIONS: We found that colonic epithelium tissues from patients with IBS have increased translocation of commensal and pathogenic live bacteria compared with controls. The mechanisms of increased translocation include MCs and VIP.
[Mh] Termos MeSH primário: Translocação Bacteriana
Colo/microbiologia
Escherichia coli/fisiologia
Mucosa Intestinal/microbiologia
Síndrome do Intestino Irritável/microbiologia
Mastócitos/microbiologia
Salmonella typhimurium/fisiologia
Peptídeo Intestinal Vasoativo/metabolismo
[Mh] Termos MeSH secundário: Adulto
Biópsia
Estudos de Casos e Controles
Colo/ultraestrutura
Disbiose
Impedância Elétrica
Escherichia coli/patogenicidade
Feminino
Imunofluorescência
Microbioma Gastrointestinal
Seres Humanos
Mucosa Intestinal/ultraestrutura
Síndrome do Intestino Irritável/diagnóstico
Síndrome do Intestino Irritável/metabolismo
Mastócitos/metabolismo
Mastócitos/ultraestrutura
Microscopia Confocal
Microscopia Eletrônica de Transmissão
Meia-Idade
Receptores Tipo II de Peptídeo Intestinal Vasoativo/metabolismo
Receptores Tipo I de Polipeptídeo Intestinal Vasoativo/metabolismo
Salmonella typhimurium/patogenicidade
Simbiose
Junções Íntimas/microbiologia
Junções Íntimas/ultraestrutura
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Vasoactive Intestinal Peptide, Type II); 0 (Receptors, Vasoactive Intestinal Polypeptide, Type I); 37221-79-7 (Vasoactive Intestinal Peptide)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170717
[St] Status:MEDLINE


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[PMID]:28356733
[Au] Autor:Zhao SJ; Wang DH; Li YW; Han L; Xiao X; Ma M; Wan DC; Hong A; Ma Y
[Ad] Endereço:Institute of Biomedicine, Department of Cellular Biology, Jinan University; National Engineering Research Center of Genetic Medicine, Key Laboratory of Bioengineering Medicine of Guangdong Province, Jinan University.
[Ti] Título:A novel selective VPAC2 agonist peptide-conjugated chitosan modified selenium nanoparticles with enhanced anti-type 2 diabetes synergy effects.
[So] Source:Int J Nanomedicine;12:2143-2160, 2017.
[Is] ISSN:1178-2013
[Cp] País de publicação:New Zealand
[La] Idioma:eng
[Ab] Resumo:A novel neuroendocrine peptide, pituitary adenylate cyclase activating peptide (PACAP), was found to have an important role in carbohydrate or lipid metabolism and was susceptible to dipeptidyl peptidase IV degradation. It can not only mediate glucose-dependent insulin secretion and lower blood glucose by activating VPAC2 receptor, but also raise blood glucose by promoting glucagon production by VPAC1 receptor activation. Therefore, its therapeutic application is restricted by the exceedingly short-acting half-life and the stimulatory function for glycogenolysis. Herein, we generated novel peptide-conjugated selenium nanoparticles (SeNPs; named as SCD), comprising a 32-amino acid PACAP-derived peptide DBAYL that selectively binds to VPAC2, and chitosan-modified SeNPs (SeNPs-CTS, SC) as slow-release carrier. The circulating half-life of SCD is 14.12 h in mice, which is 168.4-and 7.1-fold longer than wild PACAP (~5 min) and DBAYL (~1.98 h), respectively. SCD (10 nmol/L) significantly promotes INS-1 cell proliferation, glucose uptake, insulin secretion, insulin receptor expression and also obviously reduces intracellular reactive oxygen species levels in H O -injured INS-1 cells. Furthermore, the biological effects of SCD are stronger than Exendin-4 (a clinically approved drug through its insulinotropic effect), DBAYL, SeNPs or SC. A single injection of SCD (20 nmol/kg) into db/db mice with type 2 diabetes leads to enhanced insulin secretion and sustained hypoglycemic effect, and the effectiveness and duration of SCD in enhancing insulin secretion and reducing blood glucose levels are much stronger than Exendin-4, SeNPs or SC. In db/db mice, chronic administration of SCD by daily injection for 12 weeks markedly improved glucose and lipid profiles, insulin sensitivity and the structures of pancreatic and adipose tissue. The results indicate that SC can play a role as a carrier for the slow release of bioactive peptides and SCD could be a hopeful therapeutic against type 2 diabetes through the synergy effects of DBAYL and SeNPs.
[Mh] Termos MeSH primário: Quitosana/química
Diabetes Mellitus Tipo 2/tratamento farmacológico
Nanopartículas/química
Peptídeos/uso terapêutico
Receptores Tipo II de Peptídeo Intestinal Vasoativo/agonistas
Selênio/química
[Mh] Termos MeSH secundário: Animais
Glicemia/metabolismo
Proliferação Celular/efeitos dos fármacos
Diabetes Mellitus Tipo 2/patologia
Liberação Controlada de Fármacos
Jejum/sangue
Glucose/metabolismo
Glucose/farmacologia
Meia-Vida
Peróxido de Hidrogênio/toxicidade
Insulina/genética
Insulina/metabolismo
Resistência à Insulina
Masculino
Camundongos
Peptídeos/farmacologia
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Receptor de Insulina/metabolismo
Peçonhas/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Insulin); 0 (Peptides); 0 (RNA, Messenger); 0 (Reactive Oxygen Species); 0 (Receptors, Vasoactive Intestinal Peptide, Type II); 0 (Venoms); 9012-76-4 (Chitosan); 9P1872D4OL (exenatide); BBX060AN9V (Hydrogen Peroxide); EC 2.7.10.1 (Receptor, Insulin); H6241UJ22B (Selenium); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170522
[Lr] Data última revisão:
170522
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170331
[St] Status:MEDLINE
[do] DOI:10.2147/IJN.S130566


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[PMID]:28075510
[Au] Autor:Trabulsi EJ; Tripathi SK; Gomella L; Solomides C; Wickstrom E; Thakur ML
[Ad] Endereço:Department of Urology, Thomas Jefferson University, Philadelphia, PA, USA.
[Ti] Título:Development of a voided urine assay for detecting prostate cancer non-invasively: a pilot study.
[So] Source:BJU Int;119(6):885-895, 2017 Jun.
[Is] ISSN:1464-410X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To validate a hypothesis that prostate cancer can be detected non-invasively by a simple and reliable assay by targeting genomic VPAC receptors expressed on malignant prostate cancer cells shed in voided urine. PATIENTS/SUBJECTS AND METHODS: VPAC receptors were targeted with a specific biomolecule, TP4303, developed in our laboratory. With an Institutional Review Board exempt approval of use of de-identified discarded samples, an aliquot of urine collected as a standard of care, from patients presenting to the urology clinic (207 patients, 176 men and 31 women, aged ≥21 years) was cytospun. The cells were fixed and treated with TP4303 and 4,6-diamidino-2-phenylindole (DAPI). The cells were then observed under a microscope and cells with TP4303 orange fluorescence around the blue (DAPI) nucleus were considered 'malignant' and those only with a blue nucleus were regarded as 'normal'. VPAC presence was validated using receptor blocking assay and cell malignancy was confirmed by prostate cancer gene profile examination. RESULTS: The urine specimens were labelled only with gender and presenting diagnosis, with no personal health identifiers or other clinical data. The assay detected VPAC positive cells in 98.6% of the men with a prostate cancer diagnosis (141), and none of the 10 men with benign prostatic hyperplasia. Of the 56 'normal' patients, 62.5% (35 patients, 10 men and 25 women) were negative for VPAC cells; 19.6% (11, 11 men and no women) had VPAC positive cells; and 17.8% (10, four men and six women) were uninterpretable due to excessive crystals in the urine. Although data are limited, the sensitivity of the assay was 99.3% with a confidence interval (CI) of 96.1-100% and the specificity was 100% with a CI of 69.2-100%. Receptor blocking assay and fluorescence-activated cell sorting (FACS) analyses demonstrated the presence of VPAC receptors and gene profiling examinations confirmed that the cells expressing VPAC receptors were malignant prostate cancer cells. CONCLUSION: These preliminary data are highly encouraging and warrant further evaluation of the assay to serve as a simple and reliable tool to detect prostate cancer non-invasively.
[Mh] Termos MeSH primário: Neoplasias da Próstata/diagnóstico
Neoplasias da Próstata/urina
Receptores Tipo II de Peptídeo Intestinal Vasoativo/análise
Receptores Tipo I de Polipeptídeo Intestinal Vasoativo/análise
[Mh] Termos MeSH secundário: Adulto
Feminino
Seres Humanos
Masculino
Projetos Piloto
Urinálise/métodos
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; VALIDATION STUDIES
[Nm] Nome de substância:
0 (Receptors, Vasoactive Intestinal Peptide, Type II); 0 (Receptors, Vasoactive Intestinal Polypeptide, Type I)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170630
[Lr] Data última revisão:
170630
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170112
[St] Status:MEDLINE
[do] DOI:10.1111/bju.13775


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[PMID]:27816700
[Au] Autor:Pecoraro V; Sardone LM; Chisari M; Licata F; Li Volsi G; Perciavalle V; Ciranna L; Costa L
[Ad] Endereço:Instituto de Neurociencias, Consejo Superior de Investigaciones Científicas, Universidad Miguel Hernández de Elche, San Juan de Alicante, Spain.
[Ti] Título:A subnanomolar concentration of Pituitary Adenylate Cyclase-Activating Polypeptide (PACAP) pre-synaptically modulates glutamatergic transmission in the rat hippocampus acting through acetylcholine.
[So] Source:Neuroscience;340:551-562, 2017 Jan 06.
[Is] ISSN:1873-7544
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The neuropeptide PACAP modulates synaptic transmission in the hippocampus exerting multiple effects through different receptor subtypes: the underlying mechanisms have not yet been completely elucidated. The neurotransmitter acetylcholine (ACh) also exerts a well-documented modulation of hippocampal synaptic transmission and plasticity. Since PACAP was shown to stimulate ACh release in the hippocampus, we tested whether PACAP acting through ACh might indirectly modulate glutamate-mediated synaptic transmission at a pre- and/or at a post-synaptic level. Using patch clamp on rat hippocampal slices, we tested PACAP effects on stimulation-evoked AMPA receptor-mediated excitatory post-synaptic currents (EPSCs ) in the CA3-CA1 synapse and on spontaneous miniature EPSCs (mEPSCs) in CA1 pyramidal neurons. A subnanomolar dose of PACAP (0.5nM) decreased EPSCs amplitude, enhanced EPSC paired-pulse facilitation (PPF) and reduced mEPSC frequency, indicating a pre-synaptic decrease of glutamate release probability: these effects were abolished by simultaneous blockade of muscarinic and nicotinic ACh receptors, indicating the involvement of endogenous ACh. The effect of subnanomolar PACAP was abolished by a PAC1 receptor antagonist but not by a VPAC receptor blocker. At a higher concentration (10nM), PACAP inhibited EPSCs : this effect persisted in the presence of ACh receptor antagonists and did not involve any change in PPF or in mEPSC frequency, thus was not mediated by ACh and was exerted post- synaptically on CA1 pyramidal neurons. We suggest that a high-affinity PAC1 receptor pre-synaptically modulates hippocampal glutamatergic transmission acting through ACh. Therefore, administration of PACAP at very low doses might be envisaged in cognitive diseases with reduced cholinergic transmission.
[Mh] Termos MeSH primário: Acetilcolina/metabolismo
Ácido Glutâmico/metabolismo
Hipocampo/metabolismo
Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/metabolismo
Transmissão Sináptica/fisiologia
[Mh] Termos MeSH secundário: Animais
Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/administração & dosagem
Terminações Pré-Sinápticas/efeitos dos fármacos
Terminações Pré-Sinápticas/metabolismo
Células Piramidais/efeitos dos fármacos
Células Piramidais/metabolismo
Ratos Sprague-Dawley
Ratos Wistar
Receptores de AMPA/antagonistas & inibidores
Receptores de AMPA/metabolismo
Receptores de Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/metabolismo
Receptores Tipo II de Peptídeo Intestinal Vasoativo/metabolismo
Receptores Tipo I de Polipeptídeo Intestinal Vasoativo/metabolismo
Técnicas de Cultura de Tecidos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Pituitary Adenylate Cyclase-Activating Polypeptide); 0 (Receptors, AMPA); 0 (Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide, Type I); 0 (Receptors, Vasoactive Intestinal Peptide, Type II); 0 (Receptors, Vasoactive Intestinal Polypeptide, Type I); 3KX376GY7L (Glutamic Acid); N9YNS0M02X (Acetylcholine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161107
[St] Status:MEDLINE


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[PMID]:27453364
[Au] Autor:Sasaki S; Watanabe J; Ohtaki H; Matsumoto M; Murai N; Nakamachi T; Hannibal J; Fahrenkrug J; Hashimoto H; Watanabe H; Sueki H; Honda K; Miyazaki A; Shioda S
[Ad] Endereço:Department of Biochemistry, Showa University School of Medicine, Tokyo, Japan.
[Ti] Título:Pituitary adenylate cyclase-activating polypeptide promotes eccrine gland sweat secretion.
[So] Source:Br J Dermatol;176(2):413-422, 2017 Feb.
[Is] ISSN:1365-2133
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Sweat secretion is the major function of eccrine sweat glands; when this process is disturbed (paridrosis), serious skin problems can arise. To elucidate the causes of paridrosis, an improved understanding of the regulation, mechanisms and factors underlying sweat production is required. Pituitary adenylate cyclase-activating polypeptide (PACAP) exhibits pleiotropic functions that are mediated via its receptors [PACAP-specific receptor (PAC1R), vasoactive intestinal peptide (VIP) receptor type 1 (VPAC1R) and VPAC2R]. Although some studies have suggested a role for PACAP in the skin and several exocrine glands, the effects of PACAP on the process of eccrine sweat secretion have not been examined. OBJECTIVES: To investigate the effect of PACAP on eccrine sweat secretion. METHODS: Reverse transcriptase-polymerase chain reaction and immunostaining were used to determine the expression and localization of PACAP and its receptors in mouse and human eccrine sweat glands. We injected PACAP subcutaneously into the footpads of mice and used the starch-iodine test to visualize sweat-secreting glands. RESULTS: Immunostaining showed PACAP and PAC1R expression by secretory cells from mouse and human sweat glands. PACAP immunoreactivity was also localized in nerve fibres around eccrine sweat glands. PACAP significantly promoted sweat secretion at the injection site, and this could be blocked by the PAC1R-antagonist PACAP6-38. VIP, an agonist of VPAC1R and VPAC2R, failed to induce sweat secretion. CONCLUSIONS: This is the first report demonstrating that PACAP may play a crucial role in sweat secretion via its action on PAC1R located in eccrine sweat glands. The mechanisms underlying the role of PACAP in sweat secretion may provide new therapeutic options to combat sweating disorders.
[Mh] Termos MeSH primário: Glândulas Écrinas/secreção
Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/fisiologia
Suor/secreção
[Mh] Termos MeSH secundário: Adulto
Animais
Feminino

Seres Humanos
Masculino
Camundongos Endogâmicos C57BL
Fibras Nervosas/metabolismo
Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/metabolismo
Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/farmacologia
RNA Mensageiro/metabolismo
Receptores de Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/metabolismo
Receptores de Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/fisiologia
Receptores Tipo II de Peptídeo Intestinal Vasoativo/metabolismo
Receptores Tipo II de Peptídeo Intestinal Vasoativo/fisiologia
Receptores Tipo I de Polipeptídeo Intestinal Vasoativo/metabolismo
Receptores Tipo I de Polipeptídeo Intestinal Vasoativo/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Pituitary Adenylate Cyclase-Activating Polypeptide); 0 (RNA, Messenger); 0 (Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide); 0 (Receptors, Vasoactive Intestinal Peptide, Type II); 0 (Receptors, Vasoactive Intestinal Polypeptide, Type I)
[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:160726
[St] Status:MEDLINE
[do] DOI:10.1111/bjd.14885


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[PMID]:27381006
[Au] Autor:Carrión M; Pérez-García S; Martínez C; Juarranz Y; Estrada-Capetillo L; Puig-Kröger A; Gomariz RP; Gutiérrez-Cañas I
[Ad] Endereço:Faculty of Biology, Department of Cell Biology, Complutense University, Madrid, Spain.
[Ti] Título:VIP impairs acquisition of the macrophage proinflammatory polarization profile.
[So] Source:J Leukoc Biol;100(6):1385-1393, 2016 Dec.
[Is] ISSN:1938-3673
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:This study tested the hypothesis that vasoactive intestinal peptide (VIP) is able to modify the macrophage inflammatory profile, thus supporting its therapeutic role in autoimmune diseases. Macrophages are innate immune cells that display a variety of functions and inflammatory profiles in response to the environment that critically controls their polarization. Deregulation between the pro- and anti-inflammatory phenotypes has been involved in different pathologies. Rheumatoid arthritis (RA) is an autoimmune disease, in which macrophages are considered central effectors of synovial inflammation, displaying a proinflammatory profile. VIP is a pleiotropic neuropeptide with proven anti-inflammatory actions. As modulation of the macrophage phenotype has been implicated in the resolution of inflammatory diseases, we evaluated whether VIP is able to modulate human macrophage polarization. In vitro-polarized macrophages by GM-CSF (GM-MØ), with a proinflammatory profile, expressed higher levels of VIP receptors, vasoactive intestinal polypeptide receptors 1 and 2 (VPAC1 and VPAC2, respectively), than macrophages polarized by M-CSF (M-MØ) with anti-inflammatory activities. RA synovial macrophages, according to their GM-CSF-like polarization state, expressed both VPAC1 and VPAC2. In vitro-generated GM-MØ exposed to VIP exhibited an up-regulation of M-MØ gene marker expression, whereas their proinflammatory cytokine profile was reduced in favor of an anti-inflammatory function. Likewise, in GM-MØ, generated in the presence of VIP, VIP somehow changes the macrophages physiology profile to a less-damaging phenotype. Therefore, these results add new value to VIP as an immunomodulatory agent on inflammatory diseases.
[Mh] Termos MeSH primário: Macrófagos/efeitos dos fármacos
Receptores Tipo II de Peptídeo Intestinal Vasoativo/fisiologia
Receptores Tipo I de Polipeptídeo Intestinal Vasoativo/fisiologia
Peptídeo Intestinal Vasoativo/farmacologia
[Mh] Termos MeSH secundário: Artrite Reumatoide/patologia
Células Cultivadas
AMP Cíclico/metabolismo
Citocinas/biossíntese
Citocinas/genética
Regulação da Expressão Gênica/efeitos dos fármacos
Fator Estimulador de Colônias de Granulócitos e Macrófagos/farmacologia
Seres Humanos
Imunofenotipagem
Inflamação
Ativação de Macrófagos/efeitos dos fármacos
Fator Estimulador de Colônias de Macrófagos/farmacologia
Macrófagos/metabolismo
RNA Mensageiro/biossíntese
Receptores Tipo II de Peptídeo Intestinal Vasoativo/biossíntese
Receptores Tipo II de Peptídeo Intestinal Vasoativo/efeitos dos fármacos
Receptores Tipo II de Peptídeo Intestinal Vasoativo/genética
Receptores Tipo I de Polipeptídeo Intestinal Vasoativo/biossíntese
Receptores Tipo I de Polipeptídeo Intestinal Vasoativo/efeitos dos fármacos
Receptores Tipo I de Polipeptídeo Intestinal Vasoativo/genética
Líquido Sinovial/citologia
Regulação para Cima
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (RNA, Messenger); 0 (Receptors, Vasoactive Intestinal Peptide, Type II); 0 (Receptors, Vasoactive Intestinal Polypeptide, Type I); 37221-79-7 (Vasoactive Intestinal Peptide); 81627-83-0 (Macrophage Colony-Stimulating Factor); 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor); E0399OZS9N (Cyclic AMP)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160707
[St] Status:MEDLINE


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[PMID]:27329163
[Au] Autor:Olson KE; Bade AN; Schutt CR; Dong J; Shandler SJ; Boska MD; Mosley RL; Gendelman HE; Liu Y
[Ad] Endereço:Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, NE, USA.
[Ti] Título:Manganese-Enhanced Magnetic Resonance Imaging for Detection of Vasoactive Intestinal Peptide Receptor 2 Agonist Therapy in a Model of Parkinson's Disease.
[So] Source:Neurotherapeutics;13(3):635-46, 2016 Jul.
[Is] ISSN:1878-7479
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neuroprotective immunity is defined by transformation of T-cell polarity for therapeutic gain. For neurodegenerative disorders and specifically for Parkinson's disease (PD), granulocyte-macrophage colony stimulating factor or vasoactive intestinal peptide receptor 2 (VIPR2) agonists elicit robust anti-inflammatory microglial responses leading to neuronal sparing in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-intoxicated mice. While neurotherapeutic potential was demonstrated for PD, there remain inherent limitations in translating these inventions from the laboratory to patients. One obstacle in translating such novel neurotherapeutics centers on the availability of suitable noninvasive methods to track disease progression and therapeutic efficacy. To this end, we developed manganese-enhanced magnetic resonance imaging (MEMRI) assays as a way to track a linkage between glial activation and VIPR2 agonist (LBT-3627)-induced neuroprotective immunity for MPTP-induced nigrostriatal degeneration. Notably, LBT-3627-treated, MPTP-intoxicated mice show reduced MEMRI brain signal intensities. These changes paralleled reduced astrogliosis and resulted in sparing of nigral tyrosine hydroxylase neurons. Most importantly, the data suggest that MEMRI can be developed as a biomarker tool to monitor neurotherapeutic responses that are relevant to common neurodegenerative disorders used to improve disease outcomes.
[Mh] Termos MeSH primário: Aumento da Imagem/métodos
Imagem por Ressonância Magnética/métodos
Manganês/administração & dosagem
Oligopeptídeos/administração & dosagem
Doença de Parkinson/diagnóstico por imagem
Doença de Parkinson/tratamento farmacológico
Receptores Tipo II de Peptídeo Intestinal Vasoativo/agonistas
[Mh] Termos MeSH secundário: Animais
Encéfalo/diagnóstico por imagem
Encéfalo/efeitos dos fármacos
Neurônios Dopaminérgicos/efeitos dos fármacos
Neurônios Dopaminérgicos/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Microglia/efeitos dos fármacos
Microglia/metabolismo
Fármacos Neuroprotetores/administração & dosagem
Doença de Parkinson/imunologia
Transtornos Parkinsonianos/diagnóstico por imagem
Transtornos Parkinsonianos/tratamento farmacológico
Transtornos Parkinsonianos/imunologia
Proteínas Tirosina Quinases/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (LBT-3627); 0 (Neuroprotective Agents); 0 (Oligopeptides); 0 (Receptors, Vasoactive Intestinal Peptide, Type II); 42Z2K6ZL8P (Manganese); EC 2.7.10.1 (Protein-Tyrosine Kinases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160623
[St] Status:MEDLINE
[do] DOI:10.1007/s13311-016-0449-z


  8 / 390 MEDLINE  
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[PMID]:27194157
[Au] Autor:Clason TA; Girard BM; May V; Parsons RL
[Ad] Endereço:Department of Neurological Sciences, College of Medicine, University of Vermont, Burlington, VT, 05405, USA.
[Ti] Título:Activation of MEK/ERK Signaling by PACAP in Guinea Pig Cardiac Neurons.
[So] Source:J Mol Neurosci;59(2):309-16, 2016 Jun.
[Is] ISSN:1559-1166
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pituitary adenylate cyclase-activating polypeptide (PACAP) signaling can increase guinea pig cardiac neuron excitability in part through extracellular signal-regulated kinase (ERK) activation. The present study examined the PACAP receptors and signaling cascades that stimulate guinea pig cardiac neuron ERK signaling using confocal microscopy to quantify PACAP-induced neuronal phosphorylated ERK (pERK) immunoreactivity. PACAP and maxadilan, but not vasoactive intestinal polypeptide (VIP), increased cardiac neuron pERK, implicating primary roles for PACAP-selective PAC1 receptor (Adcyap1r1) signaling rather than VPAC receptors (Vipr1 and Vipr2) in the generation of cardiac neuron pERK. The adenylyl cyclase (AC) activator forskolin, but not the protein kinase C (PKC) activator phorbol myristate acetate (PMA), increased pERK. Also, Bim1 did not blunt PACAP activation of pERK. Together, the results suggest PAC1 receptor signal transduction via Gs/adenylyl cyclase (AC)/cAMP rather than Gq/phospholipase C (PLC) generated neuronal pERK. Activator and inhibitor studies suggested that the PACAP-mediated pERK activation was PKA-dependent rather than an exchange protein directly activated by a cAMP (EPAC), PKA-independent mechanism. The PACAP-induced pERK was inhibited by the clathrin inhibitor Pitstop2 to block receptor internalization and endosomal signaling. We propose that the PACAP-mediated MEK/ERK activation in cardiac neurons involves both AC/cAMP/PKA signaling and PAC1 receptor internalization/activation of signaling endosomes.
[Mh] Termos MeSH primário: Sistema de Sinalização das MAP Quinases
Miocárdio/metabolismo
Neurônios/metabolismo
Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/metabolismo
[Mh] Termos MeSH secundário: Adenilil Ciclases/metabolismo
Animais
Colforsina/farmacologia
AMP Cíclico/metabolismo
Proteínas Quinases Dependentes de AMP Cíclico/metabolismo
Feminino
Cobaias
Masculino
Miocárdio/citologia
Neurônios/efeitos dos fármacos
Inibidores de Proteínas Quinases/farmacologia
Receptores Tipo II de Peptídeo Intestinal Vasoativo/genética
Receptores Tipo II de Peptídeo Intestinal Vasoativo/metabolismo
Receptores Tipo I de Polipeptídeo Intestinal Vasoativo/genética
Receptores Tipo I de Polipeptídeo Intestinal Vasoativo/metabolismo
Acetato de Tetradecanoilforbol/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Pituitary Adenylate Cyclase-Activating Polypeptide); 0 (Protein Kinase Inhibitors); 0 (Receptors, Vasoactive Intestinal Peptide, Type II); 0 (Receptors, Vasoactive Intestinal Polypeptide, Type I); 0 (Vipr1 protein, mouse); 0 (Vipr2 protein, mouse); 1F7A44V6OU (Colforsin); E0399OZS9N (Cyclic AMP); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases); EC 4.6.1.1 (Adenylyl Cyclases); NI40JAQ945 (Tetradecanoylphorbol Acetate)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170601
[Lr] Data última revisão:
170601
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160520
[St] Status:MEDLINE
[do] DOI:10.1007/s12031-016-0766-z


  9 / 390 MEDLINE  
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[PMID]:27156032
[Au] Autor:Jin C; Zhou Z; Li W; Zhang F; Yuan J; Liu X; Cheng Z
[Ad] Endereço:Wuxi Mental Health Center, Nanjing Medical University, Wuxi 214151, Jiangsu Province, PR China; Jiangsu Institute of Psychology, Wuxi 214151, Jiangsu Province, PR China. Electronic address: jch1029@126.com.
[Ti] Título:Analysis of the association of VIPR2 polymorphisms with susceptibility to schizophrenia.
[So] Source:Psychiatry Res;241:104-7, 2016 Jul 30.
[Is] ISSN:1872-7123
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:In a previous study, we confirmed that copy number variants (CNVs) within the VIPR2 gene in Han Chinese individuals exhibit an increased risk of schizophrenia (SCZ). Herein, we further analyzed the association of eight tagged single nucleotide polymorphisms (tagSNPs) from the HapMap database with SCZ susceptibility. However, we found no significant positive signals in overall association and haplotypes analyses. Interestingly, significant SNP-SNP interaction signals associated with the risk of SCZ were observed using Multifactor Dimensionality Reduction (MDR) analysis. Furthermore, the 'CC' genotype of the VIPR2 gene was nominally associated with an increased risk of SCZ in male patients.
[Mh] Termos MeSH primário: Receptores Tipo II de Peptídeo Intestinal Vasoativo/genética
Esquizofrenia/genética
[Mh] Termos MeSH secundário: Adulto
China
Feminino
Predisposição Genética para Doença
Seres Humanos
Masculino
Meia-Idade
Polimorfismo de Nucleotídeo Único
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Vasoactive Intestinal Peptide, Type II); 0 (VIPR2 protein, human)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160509
[St] Status:MEDLINE


  10 / 390 MEDLINE  
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[PMID]:27059672
[Au] Autor:Bertolini M; Pretzlaff M; Sulk M; Bähr M; Gherardini J; Uchida Y; Reibelt M; Kinori M; Rossi A; Bíró T; Paus R
[Ad] Endereço:Department of Dermatology, University of Münster, Münster, Germany. marta.bertolini@ukmuenster.de.
[Ti] Título:Vasoactive intestinal peptide, whose receptor-mediated signalling may be defective in alopecia areata, provides protection from hair follicle immune privilege collapse.
[So] Source:Br J Dermatol;175(3):531-41, 2016 Sep.
[Is] ISSN:1365-2133
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Alopecia areata (AA) is an autoimmune disorder whose pathogenesis involves the collapse of the relative immune privilege (IP) of the hair follicle (HF). Given that vasoactive intestinal peptide (VIP) is an immunoinhibitory neuropeptide released by perifollicular sensory nerve fibres, which play a role in IP maintenance, it may modulate human HF-IP and thus be therapeutically relevant for AA. OBJECTIVES: To answer the following questions: Do human HFs express VIP receptors, and does their stimulation protect from or restore experimentally induced HF-IP collapse? Is VIP signalling defective in AA HFs? METHODS: Firstly, VIP and VIP receptor (VPAC1, VPAC2) expression in human scalp HFs and AA skin was assessed. In HF organ culture, we then explored whether VIP treatment can restore and/or protect from interferon-γ-induced HF-IP collapse, assessing the expression of the key IP markers by quantitative (immuno-)histomorphometry. RESULTS: Here we provide the first evidence that VIP receptors are expressed in the epithelium of healthy human HFs at the gene and protein level. Furthermore, VIP receptor protein expression, but not VIP(+) nerve fibres, is significantly downregulated in lesional hair bulbs of patients with AA, suggesting defects in VIP receptor-mediated signalling. Moreover, we show that VIP protects the HF from experimentally induced IP collapse in vitro, but does not fully restore it once collapsed. CONCLUSIONS: These pilot data suggest that insufficient VIP receptor-mediated signalling may contribute to impairing HF-IP in patients with AA, and that VIP is a promising candidate 'HF-IP guardian' that may be therapeutically exploited to inhibit the progression of AA lesions.
[Mh] Termos MeSH primário: Alopecia em Áreas/imunologia
Folículo Piloso/imunologia
Peptídeo Intestinal Vasoativo/fisiologia
[Mh] Termos MeSH secundário: Epitélio/metabolismo
Feminino
Voluntários Saudáveis
Seres Humanos
Interferon gama/farmacologia
Projetos Piloto
RNA Mensageiro/metabolismo
Receptores Tipo II de Peptídeo Intestinal Vasoativo/metabolismo
Receptores Tipo I de Polipeptídeo Intestinal Vasoativo/metabolismo
Couro Cabeludo/imunologia
Tolerância a Antígenos Próprios/imunologia
Peptídeo Intestinal Vasoativo/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Messenger); 0 (Receptors, Vasoactive Intestinal Peptide, Type II); 0 (Receptors, Vasoactive Intestinal Polypeptide, Type I); 37221-79-7 (Vasoactive Intestinal Peptide); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160410
[St] Status:MEDLINE
[do] DOI:10.1111/bjd.14645



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