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Pesquisa : D02.033.100.700.350 [Categoria DeCS]
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[PMID]:28461106
[Au] Autor:Staun-Ram E; Miller A
[Ad] Endereço:Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel.
[Ti] Título:Effector and regulatory B cells in Multiple Sclerosis.
[So] Source:Clin Immunol;184:11-25, 2017 11.
[Is] ISSN:1521-7035
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The role of B cells in the pathogenesis of Multiple Sclerosis (MS), an autoimmune neurodegenerative disease, is becoming eminent in recent years, but the specific contribution of the distinct B cell subsets remains to be elucidated. Several B cell subsets have shown regulatory, anti-inflammatory capacities in response to stimuli in vitro, as well as in the animal model of MS: Experimental Autoimmune Encephalomyelitis (EAE). However, the functional role of the B regulatory cells (Bregs) in vivo and specifically in the human disease is yet to be clarified. In the present review, we have summarized the updated information on the roles of effector and regulatory B cells in MS and the immune-modulatory effects of MS therapeutic agents on their phenotype and function.
[Mh] Termos MeSH primário: Subpopulações de Linfócitos B/imunologia
Linfócitos B Reguladores/imunologia
Encefalomielite Autoimune Experimental/imunologia
Esclerose Múltipla/imunologia
[Mh] Termos MeSH secundário: Alemtuzumab/uso terapêutico
Animais
Crotonatos/uso terapêutico
Fumarato de Dimetilo/uso terapêutico
Cloridrato de Fingolimode/uso terapêutico
Acetato de Glatiramer/uso terapêutico
Seres Humanos
Fatores Imunológicos/uso terapêutico
Imunossupressores/uso terapêutico
Interferon beta/uso terapêutico
Esclerose Múltipla/tratamento farmacológico
Natalizumab/uso terapêutico
Rituximab/uso terapêutico
Toluidinas/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Crotonates); 0 (Immunologic Factors); 0 (Immunosuppressive Agents); 0 (Natalizumab); 0 (Toluidines); 1C058IKG3B (teriflunomide); 3A189DH42V (Alemtuzumab); 4F4X42SYQ6 (Rituximab); 5M691HL4BO (Glatiramer Acetate); 77238-31-4 (Interferon-beta); FO2303MNI2 (Dimethyl Fumarate); G926EC510T (Fingolimod Hydrochloride)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180206
[Lr] Data última revisão:
180206
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE


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[PMID]:28956455
[Au] Autor:Masoudipour E; Kashanian S; Maleki N; Karamyan A; Omidfar K
[Ad] Endereço:a Department of Biology, Faculty of Science , Razi University , Kermanshah , Iran.
[Ti] Título:A novel intracellular pH-responsive formulation for FTY720 based on PEGylated graphene oxide nano-sheets.
[So] Source:Drug Dev Ind Pharm;44(1):99-108, 2018 Jan.
[Is] ISSN:1520-5762
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: This study was performed to investigate a novel pH-responsive nanocarrier based on modified nano graphene oxide (nGO) to promote the acid-triggered intracellular release of a poorly soluble drug, FTY720. METHODS: To synthesize a drug conjugated to modified nGO, first the polyethylene glycol (PEG) was conjugated to nGO, then the produced PEG-nGO was functionalized with the anticancer drug, FTY720, through amide bonding. It was characterized by the scanning electron microscopy (SEM), the atomic force microscopy (AFM), the Fourier transform infrared (FTIR) spectroscopy and the UV-vis spectroscopy. In vitro drug release of the FTY720-conjugated PEG-nGO was evaluated at pH 7.4 and 4.6 PBS at 37 °C. Furthermore, the antineoplastic action of unloaded and drug-loaded carrier against the human breast adenocarcinoma cell line MCF7 was explored using MTT and BrdU assays. RESULTS: Characterization methods indicated successful drug deposition on the surface of nGO. In vitro, drug release results revealed a significantly faster release of FTY720 from PEG-nGO at acidic pH, compared with physiological pH. The proliferation assays proved that the unloaded nGO had no significant cytotoxicity against MCF7 cells, while free FTY720- and FTY720-loaded PEG-nGO had an approximately equal cytotoxic effect on the MCF7 cells. It was found that the extended release characteristic of FTY720 was well fitted to Korsmeyer-Peppas model and the release profile of FTY720 from PEG-nGO is diffusion controlled. CONCLUSION: PEGylated GO can act as a pH-responsive drug carrier to improve the efficacy of anticancer drug delivery.
[Mh] Termos MeSH primário: Antineoplásicos/química
Grafite/química
Polietilenoglicóis/química
[Mh] Termos MeSH secundário: Antineoplásicos/farmacologia
Química Farmacêutica
Sistemas de Liberação de Medicamentos
Cloridrato de Fingolimode
Seres Humanos
Concentração de Íons de Hidrogênio
Células MCF-7
Microscopia de Força Atômica
Espectroscopia de Infravermelho com Transformada de Fourier
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 30IQX730WE (Polyethylene Glycols); 7782-42-5 (Graphite); G926EC510T (Fingolimod Hydrochloride)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180111
[Lr] Data última revisão:
180111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170929
[St] Status:MEDLINE
[do] DOI:10.1080/03639045.2017.1386194


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[PMID]:29186197
[Au] Autor:Li X; Wang MH; Qin C; Fan WH; Tian DS; Liu JL
[Ad] Endereço:Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
[Ti] Título:Fingolimod suppresses neuronal autophagy through the mTOR/p70S6K pathway and alleviates ischemic brain damage in mice.
[So] Source:PLoS One;12(11):e0188748, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The bioactive, signaling lipid, sphingosine-1-phosphate (S1P), and its analog, fingolimod (FTY720), have previously shown neuroprotective effects against ischemic brain injury. However, the underlying mechanisms have not yet been fully clarified. The roles of autophagy in ischemic stroke are being increasingly recognized. In the present study, we sought to determine whether the S1P pathway is involved in neuronal autophagy and investigate its possible mechanisms following stroke. Interestingly, we found that FTY720 significantly attenuates infarct volumes and reduces neuronal apoptosis on days 1 and 3 post stroke, accompanied by amelioration of functional deficits. Additionally, FTY720 was found to decrease the induction of autophagosome proteins, microtubule-associated protein 1 light chain 3(LC3-II) and Beclin1, following ischemic stroke in a dose-dependent manner. Meanwhile, protein levels of the mammalian target of rapamycin (mTOR) and the 70-kDa ribosomal protein, S6 kinase1 (p70S6K), were also up-regulated in FTY720-treated animals, and the nonspecific SphK inhibitor, N,N-dimethylsphingosine (DMS), was found to cause a reverse effect. Our results indicate that modulation of the S1P signaling pathway by FTY720 could effectively decrease neuronal autophagy through the mTOR/p70S6K pathway and attenuate ischemic brain injury in mice.
[Mh] Termos MeSH primário: Autofagia/efeitos dos fármacos
Isquemia Encefálica/patologia
Cloridrato de Fingolimode/farmacologia
Neurônios/efeitos dos fármacos
Fármacos Neuroprotetores/farmacologia
Proteínas Quinases S6 Ribossômicas 70-kDa/metabolismo
Serina-Treonina Quinases TOR/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Comportamento Animal
Isquemia Encefálica/enzimologia
Isquemia Encefálica/etiologia
Isquemia Encefálica/metabolismo
Relação Dose-Resposta a Droga
Imagem por Ressonância Magnética
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Transdução de Sinais/efeitos dos fármacos
Trombose/complicações
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neuroprotective Agents); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.1.1 (mTOR protein, mouse); EC 2.7.11.1 (Ribosomal Protein S6 Kinases, 70-kDa); G926EC510T (Fingolimod Hydrochloride)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180101
[Lr] Data última revisão:
180101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171130
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188748


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[PMID]:29214311
[Au] Autor:Xiao W; Fu S; Xu K; Feng R; Sun F; Ye W
[Ad] Endereço:Department of Ophthalmology, Huashan Hospital, Fudan University, Shanghai, China.
[Ti] Título:Fingolimod Suppresses a Cascade of Core Vicious Cycle in Dry Eye NOD Mouse Model: Involvement of Sphingosine-1-Phosphate Receptors in Infiltrating Leukocytes.
[So] Source:Invest Ophthalmol Vis Sci;58(14):6123-6132, 2017 Dec 01.
[Is] ISSN:1552-5783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose: The purpose of this study was to evaluate the inhibitory mechanism of fingolimod and the involvement of sphingosine-1-phosphate receptors (S1PRs) and cytokines-matrix metalloproteinases (MMPs)/MAP kinases (MAPKs) signaling in a dry eye disease (DED) mouse model. Methods: Sixty-four male NOD mice (DED model) and 16 age-matched BALB/c mice were used. In a preliminary experiment, 16 NOD mice were randomly divided into a positive control group and fingolimod-treated groups, with 8 BALB/c mice serving as wild-type control. In a subsequent, separate study, 48 NOD mice were randomly divided into 6 groups: fingolimod-treated groups at three different concentrations (0.05%, 0.005%, and 0.001%), normal saline group, untreated group, and fingolimod+W146 group. Animals received normal saline or fingolimod eyedrops three times daily until euthanasia 2 months later. Mice in the fingolimod+W146 group received daily intraperitoneal injections of W146 (0.1 mg/kg/day). Proinflammatory mediators were assessed by a protein array. Activities of MMP-2 and MMP-9 were evaluated by zymography. MAPKs and S1PRs were examined by Western blots and immunohistochemistry. Infiltrating cells and inhibitory mechanisms were assessed. Results: In the positive control group, levels of inflammatory mediators and S1PRs were upregulated. By comparison, fingolimod treatment significantly suppressed such markers which were significantly reversed by W146 (P < 0.01). Importantly, by double immunofluorescence staining, leukocytes were confirmed involved in DED in the NOD mouse model. Conclusions: Leukocytes are involved in DED in the NOD mouse model. The therapeutic mechanisms of fingolimod may be associated with inhibitory roles of "cytokines-MMPs/MAPKs" cycle in NOD mouse ocular surface tissues by mediating S1PRs in infiltrating leukocytes.
[Mh] Termos MeSH primário: Síndromes do Olho Seco/tratamento farmacológico
Cloridrato de Fingolimode/farmacologia
Leucócitos/metabolismo
Receptores de Lisoesfingolipídeo/metabolismo
[Mh] Termos MeSH secundário: Animais
Western Blotting
Modelos Animais de Doenças
Síndromes do Olho Seco/metabolismo
Síndromes do Olho Seco/patologia
Imuno-Histoquímica
Imunossupressores/farmacologia
Leucócitos/patologia
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos NOD
Esfingosina
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Immunosuppressive Agents); 0 (Receptors, Lysosphingolipid); G926EC510T (Fingolimod Hydrochloride); NGZ37HRE42 (Sphingosine)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171215
[Lr] Data última revisão:
171215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171208
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.17-21445


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[PMID]:28658504
[Au] Autor:Tian T; Zhang J; Zhu X; Wen S; Shi D; Zhou H
[Ad] Endereço:Department of Immunology, Nanjing Medical University, Nanjing, China.
[Ti] Título:FTY720 ameliorates renal fibrosis by simultaneously affecting leucocyte recruitment and TGF-ß signalling in fibroblasts.
[So] Source:Clin Exp Immunol;190(1):68-78, 2017 Oct.
[Is] ISSN:1365-2249
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Renal fibrosis is the common final manifestation of chronic kidney diseases and usually results in end-stage renal failure. In this study, we evaluated the effect of fingolimod (FTY720), an analogue of sphingosine 1-phosphate (S1P), as a treatment for the unilateral ureteral obstruction (UUO)-induced renal fibrosis animal model. We treated mice with FTY720 at a dosage of 1 mg/kg/day by intragastric administration from day 1 until day 7. The control group received the same amount of saline. FTY720 reduced significantly the urine albumin/creatinine ratio (UACR) in treated UUO mice. FTY720 treatment also caused a significant decrease in interstitial expansion and collagen deposition in the kidney, accompanied by reduced mononuclear cell recruitment and inflammatory cytokine expression. In addition, the expression levels of the endothelial cell adhesion molecules P-selectin and vascular cell adhesion protein 1 (VCAM-1) were suppressed in the ligated kidney by FTY720 administration, suggesting reduced renal endothelial cell activation. Furthermore, in renal interstitial fibroblast normal rat kidney (NRK)-49F cells, FTY720 significantly affected transforming growth factor (TGF)-ß-induced α-smooth muscle actin (SMA) expression and collagen synthesis by inhibiting both the Mothers against decapentaplegic homologue (Smad)2/3 and phosphatidylinositol 3-kinase/protein kinase B/glycogen synthase kinase 3 beta (PI3K/AKT/GSK3ß) signalling pathways. S1P1 knock-down by siRNA reversed this effect significantly in our fibroblast cell culture model. Therefore, FTY720 attenuates renal fibrosis via two different mechanisms: first, FTY720 suppresses the synthesis of extracellular matrix in interstitial fibroblasts by interfering with TGF-ß signalling; and secondly, FTY720 affects endothelial cell activation and chemokine expression, thereby reducing immune cell recruitment into the kidney.
[Mh] Termos MeSH primário: Fibroblastos/efeitos dos fármacos
Cloridrato de Fingolimode/uso terapêutico
Imunossupressores/uso terapêutico
Rim/efeitos dos fármacos
Leucócitos/efeitos dos fármacos
Fator de Crescimento Transformador beta/metabolismo
Obstrução Ureteral/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Adesão Celular/efeitos dos fármacos
Linhagem Celular
Movimento Celular/efeitos dos fármacos
Creatinina/urina
Matriz Extracelular/metabolismo
Fibroblastos/imunologia
Fibrose
Seres Humanos
Rim/metabolismo
Rim/patologia
Leucócitos/imunologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
RNA Interferente Pequeno/genética
Ratos
Receptores de Lisoesfingolipídeo/genética
Receptores de Lisoesfingolipídeo/metabolismo
Transdução de Sinais/efeitos dos fármacos
Obstrução Ureteral/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Immunosuppressive Agents); 0 (RNA, Small Interfering); 0 (Receptors, Lysosphingolipid); 0 (Transforming Growth Factor beta); AYI8EX34EU (Creatinine); G926EC510T (Fingolimod Hydrochloride)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170629
[St] Status:MEDLINE
[do] DOI:10.1111/cei.13003


  6 / 1653 MEDLINE  
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[PMID]:28641684
[Au] Autor:McLaughlin MF; Donoviel DB; Jones JA
[Ti] Título:Novel Indications for Commonly Used Medications as Radiation Protectants in Spaceflight.
[So] Source:Aerosp Med Hum Perform;88(7):665-676, 2017 Jul 01.
[Is] ISSN:2375-6314
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: In the space environment, the traditional radioprotective principles of time, distance, and shielding become difficult to implement. Additionally, the complex radiation environment inherent in space, the chronic exposure timeframe, and the presence of numerous confounding variables complicate the process of creating appropriate risk models for astronaut exposure. Pharmaceutical options hold tremendous promise to attenuate acute and late effects of radiation exposure in the astronaut population. Pharmaceuticals currently approved for other indications may also offer radiation protection, modulation, or mitigation properties along with a well-established safety profile. Currently there are only three agents which have been clinically approved to be employed for radiation exposure, and these only for very narrow indications. This review identifies a number of agents currently approved by the U.S. Food and Drug Administration (FDA) which could warrant further investigation for use in astronauts. Specifically, we examine preclinical and clinical evidence for statins, nonsteroidal anti-inflammatory drugs (NSAIDs), angiotensin converting enzyme inhibitors (ACEIs), angiotensin II receptor blockers (ARBs), metformin, calcium channel blockers, ß adrenergic receptor blockers, fingolimod, N-acetylcysteine, and pentoxifylline as potential radiation countermeasures.McLaughlin MF, Donoviel DB, Jones JA. Novel indications for commonly used medications as radiation protectants in spaceflight. Aerosp Med Hum Perform. 2017; 88(7):665-676.
[Mh] Termos MeSH primário: Astronautas
Lesões por Radiação/prevenção & controle
Protetores contra Radiação/uso terapêutico
Voo Espacial
[Mh] Termos MeSH secundário: Acetilcisteína/uso terapêutico
Antagonistas Adrenérgicos beta/uso terapêutico
Medicina Aeroespacial
Antagonistas de Receptores de Angiotensina/uso terapêutico
Inibidores da Enzima Conversora de Angiotensina/uso terapêutico
Anti-Inflamatórios não Esteroides/uso terapêutico
Bloqueadores dos Canais de Cálcio/uso terapêutico
Cloridrato de Fingolimode/uso terapêutico
Depuradores de Radicais Livres/uso terapêutico
Seres Humanos
Inibidores de Hidroximetilglutaril-CoA Redutases/uso terapêutico
Hipoglicemiantes/uso terapêutico
Imunossupressores/uso terapêutico
Metformina/uso terapêutico
Pentoxifilina/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Adrenergic beta-Antagonists); 0 (Angiotensin Receptor Antagonists); 0 (Angiotensin-Converting Enzyme Inhibitors); 0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Calcium Channel Blockers); 0 (Free Radical Scavengers); 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors); 0 (Hypoglycemic Agents); 0 (Immunosuppressive Agents); 0 (Radiation-Protective Agents); 9100L32L2N (Metformin); G926EC510T (Fingolimod Hydrochloride); SD6QCT3TSU (Pentoxifylline); WYQ7N0BPYC (Acetylcysteine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170829
[Lr] Data última revisão:
170829
[Sb] Subgrupo de revista:IM; S
[Da] Data de entrada para processamento:170624
[St] Status:MEDLINE
[do] DOI:10.3357/AMHP.4735.2017


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[PMID]:28607130
[Au] Autor:Cantalupo A; Gargiulo A; Dautaj E; Liu C; Zhang Y; Hla T; Di Lorenzo A
[Ad] Endereço:From the Department of Pathology and Laboratory Medicine, Center for Vascular Biology, Weill Cornell Medicine, New York (A.C., A.G., E.D., C.L., Y.Z., T.H., A.D.L.); and Department of Pharmacy, Faculty of Pharmacy, University of Naples "Federico II", Naples, Italy (A.G.).
[Ti] Título:S1PR1 (Sphingosine-1-Phosphate Receptor 1) Signaling Regulates Blood Flow and Pressure.
[So] Source:Hypertension;70(2):426-434, 2017 Aug.
[Is] ISSN:1524-4563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Nitric oxide is one of the major endothelial-derived vasoactive factors that regulate blood pressure (BP), and the bioactive lipid mediator S1P (sphingosine-1-phosphate) is a potent activator of endothelial nitric oxide synthase through G protein-coupled receptors. Endothelial-derived S1P and the autocrine/paracrine activation of S1PR (S1P receptors) play an important role in preserving vascular functions and BP homeostasis. Furthermore, FTY720 (fingolimod), binding to 4 out of 5 S1PRs recently approved by the Food and Drug Administration to treat autoimmune conditions, induces a modest and transient decrease in heart rate in both animals and humans, suggesting that drugs targeting sphingolipid signaling affect cardiovascular functions in vivo. However, the role of specific S1P receptors in BP homeostasis remains unknown. The aim of this study is to determine the role of the key vascular S1P receptors, namely, S1PR1 and S1PR3, in BP regulation in physiological and hypertensive conditions. The specific loss of endothelial S1PR1 decreases basal and stimulated endothelial-derived nitric oxide and resets BP to a higher-than-normal value. Interestingly, we identified a novel and important role for S1PR1 signaling in flow-mediated mechanotransduction. FTY720, acting as functional antagonist of S1PR1, markedly decreases endothelial S1PR1, increases BP in control mice, and exacerbates hypertension in angiotensin II mouse model, underlining the antihypertensive functions of S1PR1 signaling. Our study identifies S1P-S1PR1-nitric oxide signaling as a new regulatory pathway in vivo of vascular relaxation to flow and BP homeostasis, providing a novel therapeutic target for the treatment of hypertension.
[Mh] Termos MeSH primário: Pressão Sanguínea/fisiologia
Cloridrato de Fingolimode/farmacologia
Hipertensão
Óxido Nítrico Sintase Tipo III/metabolismo
Óxido Nítrico/metabolismo
Receptores de Lisoesfingolipídeo
[Mh] Termos MeSH secundário: Animais
Pressão Sanguínea/efeitos dos fármacos
Modelos Animais de Doenças
Células Endoteliais/metabolismo
Hipertensão/tratamento farmacológico
Hipertensão/metabolismo
Hipertensão/fisiopatologia
Imunossupressores/farmacologia
Camundongos
Receptores de Lisoesfingolipídeo/antagonistas & inibidores
Receptores de Lisoesfingolipídeo/metabolismo
Transdução de Sinais/efeitos dos fármacos
Transdução de Sinais/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Immunosuppressive Agents); 0 (Receptors, Lysosphingolipid); 0 (S1pr1 protein, mouse); 31C4KY9ESH (Nitric Oxide); EC 1.14.13.39 (Nitric Oxide Synthase Type III); G926EC510T (Fingolimod Hydrochloride)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170614
[St] Status:MEDLINE
[do] DOI:10.1161/HYPERTENSIONAHA.117.09088


  8 / 1653 MEDLINE  
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[PMID]:28535372
[Au] Autor:Ma S; Santhosh D; Kumar T P; Huang Z
[Ad] Endereço:Departments of Neuroscience and Neurology, University of Wisconsin-Madison, Madison, WI, 53705, USA; Program in Cellular and Molecular Biology, University of Wisconsin-Madison, Madison, WI53706, USA.
[Ti] Título:A Brain-Region-Specific Neural Pathway Regulating Germinal Matrix Angiogenesis.
[So] Source:Dev Cell;41(4):366-381.e4, 2017 May 22.
[Is] ISSN:1878-1551
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Intimate communication between neural and vascular cells is critical for normal brain development and function. Germinal matrix (GM), a key primordium for the brain reward circuitry, is unique among brain regions for its distinct pace of angiogenesis and selective vulnerability to hemorrhage during development. A major neonatal condition, GM hemorrhage can lead to cerebral palsy, hydrocephalus, and mental retardation. Here we identify a brain-region-specific neural progenitor-based signaling pathway dedicated to regulating GM vessel development. This pathway consists of cell-surface sphingosine-1-phosphate receptors, an intracellular cascade including Gα co-factor Ric8a and p38 MAPK, and target gene integrin ß8, which in turn regulates vascular TGF-ß signaling. These findings provide insights into region-specific specialization of neurovascular communication, with special implications for deciphering potent early-life endocrine, as well as potential gut microbiota impacts on brain reward circuitry. They also identify tissue-specific molecular targets for GM hemorrhage intervention.
[Mh] Termos MeSH primário: Encéfalo/irrigação sanguínea
Encéfalo/metabolismo
Neovascularização Fisiológica
Vias Neurais/metabolismo
[Mh] Termos MeSH secundário: Embrião de Mamíferos/irrigação sanguínea
Embrião de Mamíferos/metabolismo
Embrião de Mamíferos/patologia
Ativação Enzimática/efeitos dos fármacos
Cloridrato de Fingolimode/farmacologia
Fatores de Troca do Nucleotídeo Guanina/genética
Hemorragia/patologia
Seres Humanos
Cadeias beta de Integrinas/metabolismo
Lisofosfolipídeos/metabolismo
Mutação/genética
Neostriado/efeitos dos fármacos
Neostriado/patologia
Neovascularização Fisiológica/efeitos dos fármacos
Vias Neurais/efeitos dos fármacos
Células-Tronco Neurais/efeitos dos fármacos
Células-Tronco Neurais/metabolismo
Especificidade de Órgãos/efeitos dos fármacos
Fenótipo
Receptores de Lisoesfingolipídeo/metabolismo
Recompensa
Transdução de Sinais/efeitos dos fármacos
Esfingosina/análogos & derivados
Esfingosina/metabolismo
Fator de Crescimento Transformador beta/metabolismo
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Guanine Nucleotide Exchange Factors); 0 (Integrin beta Chains); 0 (Lysophospholipids); 0 (Receptors, Lysosphingolipid); 0 (Ric8 protein, mouse); 0 (Transforming Growth Factor beta); 0 (integrin beta8); 26993-30-6 (sphingosine 1-phosphate); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases); G926EC510T (Fingolimod Hydrochloride); NGZ37HRE42 (Sphingosine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171007
[Lr] Data última revisão:
171007
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170524
[St] Status:MEDLINE


  9 / 1653 MEDLINE  
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[PMID]:28533445
[Au] Autor:Wilk MM; Misiak A; McManus RM; Allen AC; Lynch MA; Mills KHG
[Ad] Endereço:School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin 2, Ireland; and.
[Ti] Título:Lung CD4 Tissue-Resident Memory T Cells Mediate Adaptive Immunity Induced by Previous Infection of Mice with .
[So] Source:J Immunol;199(1):233-243, 2017 Jul 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Th1 and Th17 cells have an established role in protective immunity to , but this evidence is based largely on peripheral T cells. There is emerging evidence that local tissue-resident memory T (T ) cells that accumulate in tissue following mucosal infection may be crucial for long-term immunity. In this study, we examined the role of respiratory CD4 T cells in immunity to Natural immunity to induced by infection is considered long lasting and effective at preventing reinfection. Consistent with this, we found that convalescent mice rapidly cleared the bacteria after reinfection. Furthermore, CD4 T cells with a T cell phenotype (CD44 CD62L CD69 or CD44 CD62L CD69 CD103 ) accumulated in the lungs of mice during infection with and significantly expanded through local proliferation following reinfection. These CD4 T cells were specific and secreted IL-17 or IL-17 and IFN-γ. Treatment of mice with FTY720, which prevented migration of T and B cells from lymph nodes to the circulation, significantly exacerbated infection. This was associated with significantly reduced infiltration of central memory T cells and B cells into the lungs. However, the local expansion of T cells and the associated rapid clearance of the secondary infection were not affected by treatment with FTY720 before rechallenge. Moreover, adoptive transfer of lung CD4 T cells conferred protection in naive mice. Our findings reveal that Ag-specific CD4 T cells play a critical role in adaptive immunity against reinfection and memory induced by natural infection with .
[Mh] Termos MeSH primário: Imunidade Adaptativa
Bordetella pertussis/imunologia
Linfócitos T CD4-Positivos/imunologia
Imunidade Inata
Memória Imunológica
Pulmão/imunologia
[Mh] Termos MeSH secundário: Transferência Adotiva
Animais
Linfócitos B/imunologia
Proliferação Celular
Cloridrato de Fingolimode/administração & dosagem
Interferon gama/imunologia
Interferon gama/secreção
Interleucina-17/imunologia
Interleucina-17/secreção
Pulmão/microbiologia
Pulmão/patologia
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-17); 82115-62-6 (Interferon-gamma); G926EC510T (Fingolimod Hydrochloride)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170927
[Lr] Data última revisão:
170927
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170524
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1602051


  10 / 1653 MEDLINE  
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[PMID]:28475587
[Au] Autor:Alsop J; Medin J; Cornelissen C; Vormfelde SV; Ziemssen T
[Ad] Endereço:Numerus Ltd, Wokingham, United Kingdom.
[Ti] Título:Two studies in one: A propensity-score-matched comparison of fingolimod versus interferons and glatiramer acetate using real-world data from the independent German studies, PANGAEA and PEARL.
[So] Source:PLoS One;12(5):e0173353, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: This study compared outcomes following fingolimod or BRACE treatments (beta-interferons/glatiramer acetate) in patients with active MS (≥ 1 relapse in the previous year) following previous BRACE treatment. METHODS AND FINDINGS: Patients with active MS who previously received BRACE were identified from German prospective, observational studies, PANGAEA and PEARL. A novel methodology was developed to compare outcomes between propensity-score-matched cohorts (3:1 ratio) from the independent single-arm studies. Patients in PANGAEA (n = 1287) experienced 48% fewer relapses per year than those in PEARL (n = 429; annualized relapse rate ratio: 0.52; p < 0.001). The risk of 3-month or 6-month confirmed disability progression (CDP) was reduced in PANGAEA versus PEARL (3-month: 37% reduction; hazard ratio [HR], 0.63; p < 0.001; 6-month: 47% reduction; HR, 0.53; p < 0.001). A higher proportion of patients in PANGAEA (n = 1234) than PEARL (n = 401) were free from relapses and 3-month (65.7% vs 38.7%; p < 0.001) or 6-month (68.2% vs 39.2%; p < 0.001) CDP. The probability of confirmed disability improvement was higher in PANGAEA (n = 1163) than PEARL (n = 372; 3-month: 175% increase; HR, 2.75; p < 0.001; 6-month: 126% increase; HR, 2.26; p < 0.001). Patients in PANGAEA (n = 149) were less likely than those in PEARL (n = 307) to have taken sick leave (proportion with 0 days off work: 62.4% vs 44.6%; p = 0.0005). For change in disease severity from baseline (assessed by clinicians using the Clinical Global Impressions scale; PANGAEA, n = 1207; PEARL, n = 427), a larger proportion of patients had subjective improvement and a smaller proportion had worsening status in PANGAEA than PEARL (improvement: 28.2% vs 15.2%; worsening: 16.4% vs 30.4%; p < 0.0001). CONCLUSIONS: Fingolimod appears to be more effective than BRACE in improving clinical and physician-/patient-reported outcomes in individuals with active MS.
[Mh] Termos MeSH primário: Cloridrato de Fingolimode/uso terapêutico
Acetato de Glatiramer/uso terapêutico
Interferons/uso terapêutico
Esclerose Múltipla/tratamento farmacológico
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Idoso de 80 Anos ou mais
Estudos de Coortes
Progressão da Doença
Feminino
Alemanha
Seres Humanos
Masculino
Meia-Idade
Esclerose Múltipla/patologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
5M691HL4BO (Glatiramer Acetate); 9008-11-1 (Interferons); G926EC510T (Fingolimod Hydrochloride)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170915
[Lr] Data última revisão:
170915
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170506
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0173353



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