Base de dados : MEDLINE
Pesquisa : G04.085.100 [Categoria DeCS]
Referências encontradas : 2903 [refinar]
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  1 / 2903 MEDLINE  
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[PMID]:29330456
[Au] Autor:Tunaru S; Bonnavion R; Brandenburger I; Preussner J; Thomas D; Scholich K; Offermanns S
[Ad] Endereço:Max Planck Institute for Heart and Lung Research, Department of Pharmacology, Ludwigstr. 43, 61231, Bad Nauheim, Germany.
[Ti] Título:20-HETE promotes glucose-stimulated insulin secretion in an autocrine manner through FFAR1.
[So] Source:Nat Commun;9(1):177, 2018 01 12.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The long-chain fatty acid receptor FFAR1 is highly expressed in pancreatic ß-cells. Synthetic FFAR1 agonists can be used as antidiabetic drugs to promote glucose-stimulated insulin secretion (GSIS). However, the physiological role of FFAR1 in ß-cells remains poorly understood. Here we show that 20-HETE activates FFAR1 and promotes GSIS via FFAR1 with higher potency and efficacy than dietary fatty acids such as palmitic, linoleic, and α-linolenic acid. Murine and human ß-cells produce 20-HETE, and the ω-hydroxylase-mediated formation and release of 20-HETE is strongly stimulated by glucose. Pharmacological inhibition of 20-HETE formation and blockade of FFAR1 in islets inhibits GSIS. In islets from type-2 diabetic humans and mice, glucose-stimulated 20-HETE formation and 20-HETE-dependent stimulation of GSIS are strongly reduced. We show that 20-HETE is an FFAR1 agonist, which functions as an autocrine positive feed-forward regulator of GSIS, and that a reduced glucose-induced 20-HETE formation contributes to inefficient GSIS in type-2 diabetes.
[Mh] Termos MeSH primário: Glucose/farmacologia
Ácidos Hidroxieicosatetraenoicos/metabolismo
Células Secretoras de Insulina/efeitos dos fármacos
Insulina/secreção
Receptores Acoplados a Proteínas-G/metabolismo
[Mh] Termos MeSH secundário: Adulto
Animais
Comunicação Autócrina/efeitos dos fármacos
Células COS
Linhagem Celular
Linhagem Celular Tumoral
Células Cultivadas
Cercopithecus aethiops
Diabetes Mellitus Tipo 2/genética
Diabetes Mellitus Tipo 2/metabolismo
Feminino
Seres Humanos
Ácidos Hidroxieicosatetraenoicos/sangue
Ácidos Hidroxieicosatetraenoicos/farmacologia
Células Secretoras de Insulina/metabolismo
Masculino
Camundongos Knockout
Camundongos Obesos
Meia-Idade
Receptores Acoplados a Proteínas-G/agonistas
Receptores Acoplados a Proteínas-G/genética
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (FFAR1 protein, human); 0 (Hydroxyeicosatetraenoic Acids); 0 (Insulin); 0 (Receptors, G-Protein-Coupled); 79551-86-3 (20-hydroxy-5,8,11,14-eicosatetraenoic acid); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180114
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02539-4


  2 / 2903 MEDLINE  
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[PMID]:29022487
[Au] Autor:Baskari S; Govatati S; Madhuri V; Nallabelli N; K PM; Naik S; Poornachandar; Balka S; Tamanam RR; Devi VR
[Ad] Endereço:1 Department of Biochemistry, Osmania University, Hyderabad, India.
[Ti] Título:Influence of autocrine growth hormone on NF-κB activation leading to epithelial-mesenchymal transition of mammary carcinoma.
[So] Source:Tumour Biol;39(10):1010428317719121, 2017 Oct.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Progression of breast cancers often depends on hormones among which human growth hormone is prominently involved in breast cancer progression. Earlier studies have reported constitutive activation of nuclear factor-κB, a key regulator of growth hormone receptor-mediated signaling pathway in breast carcinoma, but the precise molecular mechanisms are still elusive. In this study, we investigated the effect of human growth hormone on nuclear factor-κB activation and epithelial-mesenchymal transition in breast carcinoma. Our results explored that autocrine production of human growth hormone enhances cellular proliferation by the activation of nuclear factor-κB (65 kDa) and downregulation of E-cadherin expression. Furthermore, enhanced nuclear factor-κB expression significantly increases cell proliferation and diminishes apoptosis in MCF-7 cell line. Increased expression of nuclear factor-κB significantly enhances mammary carcinoma cell migration and invasion stimulated by autocrine human growth hormone, which results in epithelial-mesenchymal transition of MCF-7 cells. In conclusion, our study revealed the influence of human growth hormone on nuclear factor-κB activity and epithelial-mesenchymal transition in mammary carcinoma. Our findings will help to understand molecular role of "growth hormone-nuclear factor-κB axis" in mammary carcinogenesis which may facilitate the discovery of suitable pathway inhibitors for disease treatment.
[Mh] Termos MeSH primário: Neoplasias da Mama/genética
Caderinas/biossíntese
Transição Epitelial-Mesenquimal/genética
Hormônio do Crescimento/genética
[Mh] Termos MeSH secundário: Animais
Apoptose/genética
Comunicação Autócrina/genética
Neoplasias da Mama/metabolismo
Neoplasias da Mama/patologia
Caderinas/genética
Movimento Celular/genética
Proliferação Celular/genética
Feminino
Regulação Neoplásica da Expressão Gênica/genética
Hormônio do Crescimento/biossíntese
Seres Humanos
Células MCF-7
NF-kappa B/genética
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cadherins); 0 (NF-kappa B); 9002-72-6 (Growth Hormone)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171013
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317719121


  3 / 2903 MEDLINE  
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[PMID]:28941802
[Au] Autor:Valdivieso ÁG; Mori C; Clauzure M; Massip-Copiz M; Santa-Coloma TA
[Ad] Endereço:Institute for Biomedical Research (BIOMED, UCA-CONICET), Laboratory of Cellular and Molecular Biology, School of Medical Sciences, Pontifical Catholic University of Argentina (UCA) and The National Scientific and Technical Research Council of Argentina (CONICET), Buenos Aires, C1107AFF, Argentina.
[Ti] Título:CFTR modulates RPS27 gene expression using chloride anion as signaling effector.
[So] Source:Arch Biochem Biophys;633:103-109, 2017 Nov 01.
[Is] ISSN:1096-0384
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In Cystic Fibrosis (CF), the impairment of the CFTR channel activity leads to a variety of alterations, including differential gene expression. However, the CFTR signaling mechanisms remain unclear. Recently, culturing IB3-1 CF cells under different intracellular Cl concentrations ([Cl ] ), we observed several Cl -dependent genes and further characterized one of them as RPS27. Thus, we hypothesized that Cl might act as a signaling effector for CFTR signaling. Here, to test this idea, we study RPS27 expression in T84 cells modulating the CFTR activity by using CFTR inhibitors. First, we observed that incubation of T84 cells with increasing concentrations of the CFTR inhibitors CFTR(inh)-172 or GlyH-101 determined a progressive increase in the relative [Cl ] (using the Cl fluorescent probe SPQ). The [Cl ] rise was concomitant with a dose-dependent down-regulation of RPS27. These results imply that CFTR inhibition produce Cl accumulation and that RPS27 expression can be modulated by CFTR inhibition. Therefore, Cl behaves as a signaling effector for CFTR in the modulation of RPS27 expression. In addition, the IL-1ß receptor antagonist IL1RN or the JNK inhibitor SP600125, both restored the down-regulation of RPS27 induced by CFTRinh-172, implying a role of autocrine IL-1ß and JNK signaling downstream of Cl in RPS27 modulation.
[Mh] Termos MeSH primário: Cloretos/metabolismo
Regulador de Condutância Transmembrana em Fibrose Cística/genética
Células Epiteliais/metabolismo
Metaloproteínas/genética
Proteínas Nucleares/genética
Proteínas de Ligação a RNA/genética
Proteínas Ribossômicas/genética
Transdução de Sinais
[Mh] Termos MeSH secundário: Antracenos/farmacologia
Comunicação Autócrina
Benzoatos/farmacologia
Linhagem Celular Tumoral
Regulador de Condutância Transmembrana em Fibrose Cística/antagonistas & inibidores
Regulador de Condutância Transmembrana em Fibrose Cística/metabolismo
Células Epiteliais/citologia
Células Epiteliais/efeitos dos fármacos
Corantes Fluorescentes/metabolismo
Regulação da Expressão Gênica
Glicina/análogos & derivados
Glicina/farmacologia
Seres Humanos
Hidrazinas/farmacologia
Proteína Antagonista do Receptor de Interleucina 1/farmacologia
Interleucina-1beta/antagonistas & inibidores
Interleucina-1beta/genética
Interleucina-1beta/metabolismo
Transporte de Íons/efeitos dos fármacos
MAP Quinase Quinase 4/antagonistas & inibidores
MAP Quinase Quinase 4/genética
MAP Quinase Quinase 4/metabolismo
Metaloproteínas/metabolismo
Proteínas Nucleares/metabolismo
Inibidores de Proteínas Quinases/farmacologia
Proteínas de Ligação a RNA/metabolismo
Proteínas Ribossômicas/metabolismo
Tiazolidinas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3-((3-trifluoromethyl)phenyl)-5-((3-carboxyphenyl)methylene)-2-thioxo-4-thiazolidinone); 0 (Anthracenes); 0 (Benzoates); 0 (CFTR protein, human); 0 (Chlorides); 0 (Fluorescent Dyes); 0 (Hydrazines); 0 (IL1B protein, human); 0 (IL1RN protein, human); 0 (Interleukin 1 Receptor Antagonist Protein); 0 (Interleukin-1beta); 0 (Metalloproteins); 0 (N-(2-naphthalenyl)-((3,5-dibromo-2,4-dihydroxyphenyl)methylene)glycine hydrazide); 0 (Nuclear Proteins); 0 (Protein Kinase Inhibitors); 0 (RNA-Binding Proteins); 0 (RPS27 protein, human); 0 (Ribosomal Proteins); 0 (Thiazolidines); 126880-72-6 (Cystic Fibrosis Transmembrane Conductance Regulator); 1TW30Y2766 (pyrazolanthrone); EC 2.7.12.2 (MAP Kinase Kinase 4); TE7660XO1C (Glycine)
[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:170925
[St] Status:MEDLINE


  4 / 2903 MEDLINE  
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[PMID]:28892074
[Au] Autor:Blanchard JW; Xie J; El-Mecharrafie N; Gross S; Lee S; Lerner RA; Baldwin KK
[Ad] Endereço:Department of Molecular and Cellular Neuroscience, Dorris Neuroscience Center, The Scripps Research Institute, La Jolla, California, USA.
[Ti] Título:Replacing reprogramming factors with antibodies selected from combinatorial antibody libraries.
[So] Source:Nat Biotechnol;35(10):960-968, 2017 Oct.
[Is] ISSN:1546-1696
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The reprogramming of differentiated cells into induced pluripotent stem cells (iPSCs) is usually achieved by exogenous induction of transcription by factors acting in the nucleus. In contrast, during development, signaling pathways initiated at the membrane induce differentiation. The central idea of this study is to identify antibodies that can catalyze cellular de-differentiation and nuclear reprogramming by acting at the cell surface. We screen a lentiviral library encoding ∼100 million secreted and membrane-bound single-chain antibodies and identify antibodies that can replace either Sox2 and Myc (c-Myc) or Oct4 during reprogramming of mouse embryonic fibroblasts into iPSCs. We show that one Sox2-replacing antibody antagonizes the membrane-associated protein Basp1, thereby de-repressing nuclear factors WT1, Esrrb and Lin28a (Lin28) independent of Sox2. By manipulating this pathway, we identify three methods to generate iPSCs. Our results establish unbiased selection from autocrine combinatorial antibody libraries as a robust method to discover new biologics and uncover membrane-to-nucleus signaling pathways that regulate pluripotency and cell fate.
[Mh] Termos MeSH primário: Anticorpos/metabolismo
Reprogramação Celular
Técnicas de Química Combinatória
[Mh] Termos MeSH secundário: Animais
Comunicação Autócrina
Blastocisto/citologia
Proteínas de Ligação a Calmodulina/metabolismo
Reprogramação Celular/efeitos dos fármacos
Células Clonais
Proteínas do Citoesqueleto/metabolismo
Fibroblastos/citologia
Fibroblastos/efeitos dos fármacos
Células-Tronco Pluripotentes Induzidas/citologia
Células-Tronco Pluripotentes Induzidas/efeitos dos fármacos
Camundongos Endogâmicos C57BL
Proteínas do Tecido Nervoso/metabolismo
Fosforilação/efeitos dos fármacos
Ligação Proteica/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-myc/metabolismo
Reprodutibilidade dos Testes
Fatores de Transcrição SOXB1/metabolismo
Proteínas Smad/metabolismo
Fator de Crescimento Transformador beta/farmacologia
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies); 0 (Basp1 protein, mouse); 0 (Calmodulin-Binding Proteins); 0 (Cytoskeletal Proteins); 0 (Nerve Tissue Proteins); 0 (Proto-Oncogene Proteins c-myc); 0 (SOXB1 Transcription Factors); 0 (Smad Proteins); 0 (Transforming Growth Factor beta)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170912
[St] Status:MEDLINE
[do] DOI:10.1038/nbt.3963


  5 / 2903 MEDLINE  
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[PMID]:28887036
[Au] Autor:Chen Z; Xu L; Su T; Ke Z; Peng Z; Zhang N; Peng S; Zhang Q; Liu G; Wei G; Guo Y; He M; Kuang M
[Ad] Endereço:Department of Liver Surgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China.
[Ti] Título:Autocrine STIP1 signaling promotes tumor growth and is associated with disease outcome in hepatocellular carcinoma.
[So] Source:Biochem Biophys Res Commun;493(1):365-372, 2017 Nov 04.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Stress-induced phosphoprotein 1 (STIP1) is an adaptor protein that bridges between HSP70 and HSP90 folding and a secretory protein which regulates malignant cell growth. However, the role of STIP1 in hepatocellular carcinoma (HCC) remains unknown. Here, we found high expression of STIP1 in tumors was associated with worse overall survival (41.3 vs 62.7 months, P < 0.001) in 231 HCC patients. STIP1 was overexpressed in HCC tissues compared to adjacent non-tumor liver tissue (64.9% vs 4.0% P < 0.001), and serum STIP1 levels of HCC patients were elevated compared to healthy controls (P < 0.001). Mechanistically, STIP1 promoted HCC growth through PI3K-AKT-dependent anti-apoptotic pathway. STIP1 mediated cell growth in an autocrine fashion, which could be suppressed either by neutralizing extracellular STIP1 or by knocking down intracellular STIP1. In xenograft mouse model, knockdown of STIP1 significantly reduced tumor growth (P < 0.001). In conclusion, STIP1 is upregulated in HCC and associated with poor clinical prognosis. Blocking STIP1 activity suppresses HCC cell growth, providing the rationale for STIP1 as a potential therapeutic target in HCC.
[Mh] Termos MeSH primário: Comunicação Autócrina
Carcinoma Hepatocelular/metabolismo
Carcinoma Hepatocelular/mortalidade
Proliferação Celular
Proteínas de Choque Térmico/metabolismo
Neoplasias Hepáticas/metabolismo
Neoplasias Hepáticas/mortalidade
[Mh] Termos MeSH secundário: Idoso
Animais
Biomarcadores Tumorais/metabolismo
Carcinoma Hepatocelular/patologia
Linhagem Celular Tumoral
China/epidemiologia
Progressão da Doença
Feminino
Seres Humanos
Neoplasias Hepáticas/patologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Meia-Idade
Prevalência
Reprodutibilidade dos Testes
Fatores de Risco
Sensibilidade e Especificidade
Taxa de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Heat-Shock Proteins); 0 (STIP1 protein, human)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170910
[St] Status:MEDLINE


  6 / 2903 MEDLINE  
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[PMID]:28872459
[Au] Autor:Li B; Wang X; Choi IY; Wang YC; Liu S; Pham AT; Moon H; Smith DJ; Rao DS; Boldin MP; Yang L
[Ad] Endereço:Department of Microbiology, Immunology and Molecular Genetics.
[Ti] Título:miR-146a modulates autoreactive Th17 cell differentiation and regulates organ-specific autoimmunity.
[So] Source:J Clin Invest;127(10):3702-3716, 2017 Oct 02.
[Is] ISSN:1558-8238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Autoreactive CD4 T cells that differentiate into pathogenic Th17 cells can trigger autoimmune diseases. Therefore, investigating the regulatory network that modulates Th17 differentiation may yield important therapeutic insights. miR-146a has emerged as a critical modulator of immune reactions, but its role in regulating autoreactive Th17 cells and organ-specific autoimmunity remains largely unknown. Here, we have reported that miR-146a-deficient mice developed more severe experimental autoimmune encephalomyelitis (EAE), an animal model of human multiple sclerosis (MS). We bred miR-146a-deficient mice with 2D2 T cell receptor-Tg mice to generate 2D2 CD4 T cells that are deficient in miR-146a and specific for myelin oligodendrocyte glycoprotein (MOG), an autoantigen in the EAE model. miR-146a-deficient 2D2 T cells induced more severe EAE and were more prone to differentiate into Th17 cells. Microarray analysis revealed enhancements in IL-6- and IL-21-induced Th17 differentiation pathways in these T cells. Further study showed that miR-146a inhibited the production of autocrine IL-6 and IL-21 in 2D2 T cells, which in turn reduced their Th17 differentiation. Thus, our study identifies miR-146a as an important molecular brake that blocks the autocrine IL-6- and IL-21-induced Th17 differentiation pathways in autoreactive CD4 T cells, highlighting its potential as a therapeutic target for treating autoimmune diseases.
[Mh] Termos MeSH primário: Autoimunidade
Diferenciação Celular/imunologia
Encefalomielite Autoimune Experimental/imunologia
MicroRNAs/imunologia
Esclerose Múltipla/imunologia
Células Th17/imunologia
[Mh] Termos MeSH secundário: Animais
Comunicação Autócrina/genética
Comunicação Autócrina/imunologia
Diferenciação Celular/genética
Encefalomielite Autoimune Experimental/genética
Seres Humanos
Interleucina-6/genética
Interleucina-6/imunologia
Interleucinas/genética
Interleucinas/imunologia
Camundongos
Camundongos Knockout
MicroRNAs/genética
Esclerose Múltipla/genética
Glicoproteína Mielina-Oligodendrócito/genética
Glicoproteína Mielina-Oligodendrócito/imunologia
Especificidade de Órgãos/genética
Especificidade de Órgãos/imunologia
Células Th17/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-6); 0 (Interleukins); 0 (MicroRNAs); 0 (Mirn146 microRNA, mouse); 0 (Mog protein, mouse); 0 (Myelin-Oligodendrocyte Glycoprotein); 0 (interleukin-21); 0 (interleukin-6, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170906
[St] Status:MEDLINE


  7 / 2903 MEDLINE  
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[PMID]:28734947
[Au] Autor:Kikuchi A; Pradhan-Sundd T; Singh S; Nagarajan S; Loizos N; Monga SP
[Ad] Endereço:Department of Pathology and Medicine and Pittsburgh Liver Research Center, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania.
[Ti] Título:Platelet-Derived Growth Factor Receptor α Contributes to Human Hepatic Stellate Cell Proliferation and Migration.
[So] Source:Am J Pathol;187(10):2273-2287, 2017 Oct.
[Is] ISSN:1525-2191
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Platelet-derived growth factor receptor α (PDGFRα), a tyrosine kinase receptor, is up-regulated in hepatic stellate cells (HSCs) during chronic liver injury. HSCs mediate hepatic fibrosis through their activation from a quiescent state partially in response to profibrotic growth factors. HSC activation entails enhanced expression of profibrotic genes, increase in proliferation, and increase in motility, which facilitates migration within the hepatic lobule. We show colocalization of PDGFRα in murine carbon tetrachloride, bile duct ligation, and 0.1% 3,5-diethoxycarbonyl-1,4-dihydrocollidine models of chronic liver injury, and investigate the role of PDGFRα on proliferation, profibrotic gene expression, and migration in primary human HSCs (HHSteCs) using the PDGFRα-specific inhibitory monoclonal antibody olaratumab. Although lacking any effects on HHSteC transdifferentiation assessed by gene expression of ACTA2, TGFB1, COL1A1, SYP1, and FN1, olaratumab specifically reduced HHSteC proliferation (AlamarBlue assay) and cell migration (transwell migration assays). Using phospho-specific antibodies, we show that olaratumab attenuates PDGFRα activation in response to PDGF-BB, and reduced phosphorylation of extracellular signal-regulated kinase 1 and 2, Elk-1, p38, Akt, focal adhesion kinase, mechanistic target of rapamycin, C10 regulator of kinase II, and C10 regulator of kinase-like, suggesting that PDGFRα contributes to mitogenesis and actin reorganization through diverse downstream effectors. Our findings support a distinct contribution of PDGFRα signaling to HSC proliferation and migration and provide evidence that inhibition of PDGFRα signaling could alter the pathogenesis of hepatic fibrosis.
[Mh] Termos MeSH primário: Movimento Celular
Células Estreladas do Fígado/citologia
Células Estreladas do Fígado/metabolismo
Receptor alfa de Fator de Crescimento Derivado de Plaquetas/metabolismo
[Mh] Termos MeSH secundário: Animais
Anticorpos Monoclonais/farmacologia
Comunicação Autócrina/efeitos dos fármacos
Movimento Celular/efeitos dos fármacos
Movimento Celular/genética
Proliferação Celular/efeitos dos fármacos
Proliferação Celular/genética
Densitometria
Modelos Animais de Doenças
Regulação da Expressão Gênica/efeitos dos fármacos
Células Estreladas do Fígado/efeitos dos fármacos
Seres Humanos
Ligantes
Cirrose Hepática/genética
Cirrose Hepática/metabolismo
Cirrose Hepática/patologia
Camundongos Endogâmicos C57BL
Modelos Biológicos
Fosforilação/efeitos dos fármacos
Fator de Crescimento Derivado de Plaquetas/farmacologia
Transdução de Sinais/efeitos dos fármacos
Transdução de Sinais/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Ligands); 0 (Platelet-Derived Growth Factor); EC 2.7.10.1 (Receptor, Platelet-Derived Growth Factor alpha); TT6HN20MVF (olaratumab)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170724
[St] Status:MEDLINE


  8 / 2903 MEDLINE  
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[PMID]:28711495
[Au] Autor:Dube PR; Birnbaumer L; Vazquez G
[Ad] Endereço:Department of Physiology and Pharmacology, Center for Hypertension and Personalized Medicine, University of Toledo College of Medicine and Life Sciences, University of Toledo Health Science Campus, 3000 Transverse Dr., Toledo, OH 43614, USA.
[Ti] Título:Evidence for constitutive bone morphogenetic protein-2 secretion by M1 macrophages: Constitutive auto/paracrine osteogenic signaling by BMP-2 in M1 macrophages.
[So] Source:Biochem Biophys Res Commun;491(1):154-158, 2017 Sep 09.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mechanisms mediating vascular calcification recapitulate osteogenic processes encompassing bone formation and imply participation of bone related proteins such as bone morphogenetic protein-2 (BMP-2). Macrophages are amongst the cells that contribute to vascular ossification by releasing cytokines that induce an osteogenic program in vascular smooth muscle cells, and also by becoming themselves osteoclast-like cells. In inflammatory vascular disease, the macrophage population in the vascular wall is diverse, with the M1 or inflammatory, and the M2 or anti-inflammatory macrophage types being dominant. Yet, the osteogenic potential of M1 and M2 macrophages remains unknown. Prompted by recent studies from our laboratory showing that in macrophages the Transient Receptor Potential Canonical 3 (TRPC3) channel contributes to endoplasmic reticulum (ER) stress-induced apoptosis in M1, but not in M2 macrophages, and given the strong relationship between ER stress and vascular calcification, we wished to examine whether TRPC3 would play a role in the osteogenic signaling of polarized macrophages. The findings reported here indicate that a constitutive BMP-2-dependent signaling operates in M1 macrophages, which is not affected by deletion of Trpc3 and is not subject to regulation by ER stress. Our studies suggest operation of an auto/paracrine mechanism by which BMP-2 secreted by M1 macrophages maintains constitutive activation of a BMP-2 receptor/SMAD1/5 signaling axis.
[Mh] Termos MeSH primário: Comunicação Autócrina/fisiologia
Proteína Morfogenética Óssea 2/metabolismo
Macrófagos/metabolismo
Osteogênese/fisiologia
Comunicação Parácrina/fisiologia
Canais de Cátion TRPC/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Estresse do Retículo Endoplasmático/fisiologia
Camundongos
Camundongos Transgênicos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bmp2 protein, mouse); 0 (Bone Morphogenetic Protein 2); 0 (TRPC Cation Channels); 0 (TRPC3 cation channel)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170830
[Lr] Data última revisão:
170830
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170717
[St] Status:MEDLINE


  9 / 2903 MEDLINE  
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[PMID]:28669928
[Au] Autor:Olsavszky V; Ulbrich F; Singh S; Diett M; Sticht C; Schmid CD; Zierow J; Wohlfeil SA; Schledzewski K; Dooley S; Gaitantzi H; Breitkopf-Heinlein K; Géraud C; Goerdt S; Koch PS
[Ad] Endereço:Department of Dermatology, Venereology and Allergy, University Medical Center and Medical Faculty Mannheim, University of Heidelberg, and Center of Excellence in Dermatology, Mannheim, Germany.
[Ti] Título:GATA4 and LMO3 balance angiocrine signaling and autocrine inflammatory activation by BMP2 in liver sinusoidal endothelial cells.
[So] Source:Gene;627:491-499, 2017 Sep 05.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Liver sinusoidal endothelial cells (LSEC) represent a unique, organ-specific type of discontinuous endothelial cells. LSEC instruct the hepatic vascular niche by paracrine-acting angiocrine factors. Recently, we have shown that LSEC-specific transcriptional regulator GATA4 induces expression of BMP2 in cultured endothelial cells (EC) in vitro. Furthermore, angiocrine Bmp2 signaling in the liver in vivo was demonstrated to control iron homeostasis. Here, we investigated GATA4-dependent autocrine BMP2 signaling in endothelial cells by gene expression profiling. GATA4 induced a large cluster of inflammatory endothelial response genes in cultured EC, which is similar to previously identified virus-induced and interferon-associated responses. Treating the cells with the BMP2 inhibitor Noggin counter-regulated the GATA4-dependent inflammatory phenotype of EC, indicating that BMP2 is indeed the major driver. In contrast to continuous EC, LSEC were less prone to activation by BMP2. Notably, GATA4-dependent induction of the inflammatory EC response gene cluster was attenuated by over-expression of the LSEC-specific transcriptional modifier LMO3 while hepatocyte activation was fully preserved, indicating conserved BMP2 synthesis. In summary, our data suggest that transcriptional counter-regulation by GATA4 and LMO3 in LSEC prevents autocrine induction of an inflammatory phenotype, while maintaining angiocrine BMP2-mediated cell-cell communication in the liver vascular niche.
[Mh] Termos MeSH primário: Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Comunicação Autócrina
Proteína Morfogenética Óssea 2/metabolismo
Fator de Transcrição GATA4/metabolismo
Proteínas com Domínio LIM/metabolismo
[Mh] Termos MeSH secundário: Animais
Proteína Morfogenética Óssea 2/antagonistas & inibidores
Células Cultivadas
Hepatócitos/metabolismo
Células Endoteliais da Veia Umbilical Humana/metabolismo
Seres Humanos
Interferons/genética
Interferons/metabolismo
Fígado/irrigação sanguínea
Fígado/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (BMP2 protein, human); 0 (Bone Morphogenetic Protein 2); 0 (GATA4 Transcription Factor); 0 (GATA4 protein, human); 0 (LIM Domain Proteins); 0 (LMO3 protein, human); 9008-11-1 (Interferons)
[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:170704
[St] Status:MEDLINE


  10 / 2903 MEDLINE  
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[PMID]:28636167
[Au] Autor:Yue M; Xia Y; Shi C; Guan C; Li Y; Liu R; Wei Z; Dai Y
[Ad] Endereço:Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, Nanjing, China.
[Ti] Título:Berberine ameliorates collagen-induced arthritis in rats by suppressing Th17 cell responses via inducing cortistatin in the gut.
[So] Source:FEBS J;284(17):2786-2801, 2017 Sep.
[Is] ISSN:1742-4658
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Berberine, an isoquinoline alkaloid, has been reported to ameliorate various autoimmune diseases including rheumatoid arthritis by oral administration. However, its mechanism remains mysterious due to an extremely low bioavailability. The fact that berberine readily accumulates in the gut, the largest endocrine organ in the body, attracted us to explore its anti-arthritic mechanism in view of the induction of intestinal immunosuppressive neuropeptides. In this study, berberine (200 mg·kg , i.g.) was shown to ameliorate collagen-induced arthritis in rats, which was manifested by the reduction of clinical signs and joint destruction, as well as marked down-regulation of Th17 cell frequency and interleukin-17 level in blood. In contrast, an intravenous injection of berberine failed to affect arthritis in rats, implying that its anti-arthritic effect was gut-dependent. Further studies revealed that oral berberine selectively elevated the levels of cortistatin, of five gut-derived neuropeptides tested, in the intestines and sera of arthrititic rats. Antagonists of ghrelin/growth hormone secretagogue receptor 1 (a subtype of cortistatin receptor) almost completely abolished the ameliorative effect of berberine on arthritis and Th17 cell responses in rats. In vitro, berberine showed a moderate ability to promote the expression of cortistatin in nerve cells, which was strengthened when the nerve cells were cocultured with enteroendocrine cells to induce an autocrine/paracrine environment. In summary, oral berberine exerted anti-arthritic effect through inhibiting the Th17 cell response, which was closely associated with the induction of cortistatin generation from gut through augmenting autocrine/paracrine action between enteric nerve cells and endocrine cells.
[Mh] Termos MeSH primário: Antirreumáticos/farmacologia
Artrite Experimental/tratamento farmacológico
Berberina/farmacologia
Imunossupressores/farmacologia
Neuropeptídeos/genética
Células Th17/efeitos dos fármacos
[Mh] Termos MeSH secundário: Administração Oral
Animais
Antirreumáticos/uso terapêutico
Artrite Experimental/imunologia
Artrite Experimental/metabolismo
Comunicação Autócrina
Berberina/uso terapêutico
Avaliação Pré-Clínica de Medicamentos
Sistema Nervoso Entérico/efeitos dos fármacos
Sistema Nervoso Entérico/metabolismo
Células Enteroendócrinas/efeitos dos fármacos
Células Enteroendócrinas/metabolismo
Feminino
Imunossupressores/uso terapêutico
Intestino Delgado/efeitos dos fármacos
Neuropeptídeos/metabolismo
Células PC12
Ratos
Ratos Wistar
Células Th17/metabolismo
Ativação Transcricional/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antirheumatic Agents); 0 (Immunosuppressive Agents); 0 (Neuropeptides); 0 (cortistatin); 0I8Y3P32UF (Berberine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170622
[St] Status:MEDLINE
[do] DOI:10.1111/febs.14147



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