Base de dados : MEDLINE
Pesquisa : D02.455.426.559.847.117 [Categoria DeCS]
Referências encontradas : 5538 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 554 ir para página                         

  1 / 5538 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28592143
[Au] Autor:Pang X; Lin X; Tian Y; Liang R; Wang J; Yang B; Zhou X; Kaliyaperumal K; Luo X; Tu Z; Liu Y
[Ad] Endereço:a CAS Key Laboratory of Tropical Marine Bio-resources and Ecology/Guangdong Key Laboratory of Marine Materia Medica/RNAM Center for Marine Microbiology , South China Sea Institute of Oceanology, Chinese Academy of Sciences , Guangzhou , China.
[Ti] Título:Three new polyketides from the marine sponge-derived fungus Trichoderma sp. SCSIO41004.
[So] Source:Nat Prod Res;32(1):105-111, 2018 Jan.
[Is] ISSN:1478-6427
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Three new polyketides named trichbenzoisochromen A (1), 5,7-dihydroxy-3-methyl -2-(2-oxopropyl)naphthalene-1,4-dione (2) and 7-acetyl-1,3,6-trihydroxyanthracene-9,10- dione (3) together with six known compounds (4-9) were isolated from a sponge-derived fungus Trichoderma sp. SCSIO41004. The structures of three new polyketides (1-3) were determined by the extensive spectroscopic analysis, including 1D, 2D NMR and HRESIMS data. The absolute configuration of compound 1 was confirmed by the specific optical rotation value and CD spectra analyses. Compound 4 exhibited significant inhibitory activity against EV71 with the IC value of 25.7 µM.
[Mh] Termos MeSH primário: Antracenos/química
Antivirais/química
Antivirais/farmacologia
Naftalenos/química
Policetídeos/química
Trichoderma/química
[Mh] Termos MeSH secundário: Animais
Antracenos/farmacologia
Organismos Aquáticos/química
Dicroísmo Circular
Enterovirus Humano A/efeitos dos fármacos
Fermentação
Seres Humanos
Vírus da Influenza A Subtipo H3N2/efeitos dos fármacos
Células K562
Células MCF-7
Espectroscopia de Ressonância Magnética/métodos
Estrutura Molecular
Naftalenos/farmacologia
Policetídeos/farmacologia
Poríferos/microbiologia
Espectrometria de Massas por Ionização por Electrospray
Trichoderma/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anthracenes); 0 (Antiviral Agents); 0 (Naphthalenes); 0 (Polyketides)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170609
[St] Status:MEDLINE
[do] DOI:10.1080/14786419.2017.1338286


  2 / 5538 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29197865
[Au] Autor:Liu Y; Zhang Y; Zou J; Yan L; Yu X; Lu P; Wu X; Li Q; Gu R; Zhu D
[Ad] Endereço:Department of Biopharmaceutical Key Laboratory of Heilongjiang Province, Harbin Medical University, Harbin, China.
[Ti] Título:Andrographolide Induces Autophagic Cell Death and Inhibits Invasion and Metastasis of Human Osteosarcoma Cells in An Autophagy-Dependent Manner.
[So] Source:Cell Physiol Biochem;44(4):1396-1410, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Osteosarcoma (OS) is the most common primary malignant tumor of bone tissue. Although treatment effectiveness has improved, the OS survival rate has fluctuated in recent years. Andrographolide (AG) has been reported to have antitumor activity against a variety of tumors. Our aim was to investigate the effects and potential mechanisms of AG in human osteosarcoma. METHODS: Cell viability and morphological changes were assessed by MTT and live/dead assays. Apoptosis was detected using Annexin V-FITC/PI double staining, DAPI, and caspase-3 assays. Autophagy was detected with mRFP-GFP-LC3 adenovirus transfection and western blot. Cell migration and invasion were detected by wound healing assay and Transwell® experiments. RESULTS: AG dose-dependently reduced the viability of osteosarcoma cells. No increase in apoptosis was detected in AG-treated human OS MG-63 and U-2OS cells, and the pan-caspase inhibitor z-VAD did not attenuate AG-induced cell death. However, AG induced autophagy by suppressing PI3K/Akt/mTOR and enhancing JNK signaling pathways. 3-MA and Beclin-1 siRNA could reverse the cytotoxic effects of AG. In addition, AG inhibited the invasion and metastasis of OS, and this effect could be reversed with Beclin-1 siRNA. CONCLUSION: AG inhibits viability and induces autophagic death in OS cells. AG-induced autophagy inhibits the invasion and metastasis of OS.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Autofagia/efeitos dos fármacos
Diterpenos/toxicidade
[Mh] Termos MeSH secundário: Antracenos/farmacologia
Beclina-1/antagonistas & inibidores
Beclina-1/genética
Beclina-1/metabolismo
Neoplasias Ósseas/metabolismo
Neoplasias Ósseas/patologia
Caspase 3/metabolismo
Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Diterpenos/química
Seres Humanos
Proteínas Quinases JNK Ativadas por Mitógeno/antagonistas & inibidores
Proteínas Quinases JNK Ativadas por Mitógeno/metabolismo
Oligopeptídeos/farmacologia
Osteossarcoma/metabolismo
Osteossarcoma/patologia
Fosfatidilinositol 3-Quinases/metabolismo
Proteínas Proto-Oncogênicas c-akt/metabolismo
Interferência de RNA
RNA Interferente Pequeno/metabolismo
Transdução de Sinais/efeitos dos fármacos
Serina-Treonina Quinases TOR/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anthracenes); 0 (Beclin-1); 0 (Diterpenes); 0 (Oligopeptides); 0 (RNA, Small Interfering); 0 (benzyloxycarbonyl-valyl-alanyl-aspartic acid); 1TW30Y2766 (pyrazolanthrone); 410105JHGR (andrographolide); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.1.1 (MTOR protein, human); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases); EC 3.4.22.- (Caspase 3)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171204
[St] Status:MEDLINE
[do] DOI:10.1159/000485536


  3 / 5538 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29179205
[Au] Autor:Liu H; Jing X; Dong A; Bai B; Wang H
[Ad] Endereço:Department of Cardiology, Tangdu Hospital, the Fourth Military University, Xi'an, China.
[Ti] Título:Overexpression of TIMP3 Protects Against Cardiac Ischemia/Reperfusion Injury by Inhibiting Myocardial Apoptosis Through ROS/Mapks Pathway.
[So] Source:Cell Physiol Biochem;44(3):1011-1023, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Myocardial ischemia/reperfusion (I/R) injury remains a great challenge in clinical therapy. Tissue inhibitor of metalloproteinases 3 (TIMP3) plays a crucial role in heart physiological and pathophysiological processes. However, the effects of TIMP3 on I/R injury remain unknown. METHODS: C57BL/6 mice were infected with TIMP3 adenovirus by local delivery in myocardium followed by I/R operation or doxorubicin treatment. Neonatal rat cardiomyocytes were pretreated with TIMP3 adenovirus prior to anoxia/reoxygenation (A/R) treatment in vitro. Histology, echocardiography, in vivo phenotypical analysis, flow cytometry and western blotting were used to investigate the altered cardiac function and underlying mechanisms. RESULTS: The results showed that upregulation of TIMP3 in myocardium markedly inhibited myocardial infarct areas and the cardiac dysfunction induced by I/R or by doxorubicin treatment. TUNEL staining revealed that TIMP3 overexpression attenuated I/R-induced myocardial apoptosis, accompanied by decreased Bax/Bcl-2 ratio, Cleaved Caspase-3 and Cleaved Caspase-9 expression. In vitro, A/R-induced cardiomyocyte apoptosis was abrogated by pharmacological inhibition of reactive oxygen species (ROS) production or MAPKs signaling. Attenuation of ROS production reversed A/R-induced MAPKs activation, whereas MAPKs inhibitors showed on effect on ROS production. Furthermore, in vivo or in vitro overexpression of TIMP3 significantly inhibited I/R- or A/R-induced ROS production and MAPKs activation. CONCLUSION: Our findings demonstrate that TIMP3 upregulation protects against cardiac I/R injury through inhibiting myocardial apoptosis. The mechanism may be related to inhibition of ROS-initiated MAPKs pathway. This study suggests that TIMP3 may be a potential therapeutic target for the treatment of I/R injury.
[Mh] Termos MeSH primário: Miocárdio/metabolismo
Inibidor Tecidual de Metaloproteinase-3/metabolismo
[Mh] Termos MeSH secundário: Acetilcisteína/farmacologia
Animais
Antracenos/farmacologia
Apoptose/efeitos dos fármacos
Caspase 3/metabolismo
Caspase 9/metabolismo
Células Cultivadas
Óxidos N-Cíclicos/farmacologia
Doxorrubicina/toxicidade
Ecocardiografia
Coração/diagnóstico por imagem
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Proteínas Quinases Ativadas por Mitógeno/antagonistas & inibidores
Proteínas Quinases Ativadas por Mitógeno/metabolismo
Traumatismo por Reperfusão Miocárdica/induzido quimicamente
Traumatismo por Reperfusão Miocárdica/metabolismo
Traumatismo por Reperfusão Miocárdica/patologia
Miócitos Cardíacos/citologia
Miócitos Cardíacos/efeitos dos fármacos
Miócitos Cardíacos/metabolismo
Fosforilação/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Ratos
Ratos Sprague-Dawley
Espécies Reativas de Oxigênio/metabolismo
Transdução de Sinais/efeitos dos fármacos
Marcadores de Spin
Inibidor Tecidual de Metaloproteinase-3/genética
Proteína X Associada a bcl-2/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anthracenes); 0 (Cyclic N-Oxides); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (Reactive Oxygen Species); 0 (Spin Labels); 0 (Tissue Inhibitor of Metalloproteinase-3); 0 (bcl-2-Associated X Protein); 1TW30Y2766 (pyrazolanthrone); 80168379AG (Doxorubicin); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); EC 3.4.22.- (Caspase 3); EC 3.4.22.- (Caspase 9); U78ZX2F65X (tempol); WYQ7N0BPYC (Acetylcysteine)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1159/000485401


  4 / 5538 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28958943
[Au] Autor:Reddy GS; Mukhopadhyay AG; Dey CS
[Ad] Endereço:Kusuma School of Biological Sciences, Indian Institute of Technology Delhi, Hauz Khas, New Delhi 110016, India.
[Ti] Título:The p38 MAP kinase inhibitor, PD 169316, inhibits flagellar motility in Leishmania donovani.
[So] Source:Biochem Biophys Res Commun;493(4):1425-1429, 2017 Dec 02.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mitogen-activated protein kinases (MAPKs) have been demonstrated to regulate flagellar/ciliary motility of spermatozoa and miracidia of Schistosoma mansoni. However, the role of MAPKs in mediating flagella-driven motility of Leishmania donovani is unexplored. We investigated the function of MAPKs in motility regulation of L. donovani using pharmacological inhibitors and activators of various MAPKs and fast-capture videomicroscopy. Our studies have revealed that the inhibitor of p38 MAPK, PD 169316, significantly affected various motility parameters such as flagellar beat frequency, parasite swimming speed, waveform of the flagellum and resulted in reduced parasite motility. Together, our results suggest that a MAPK, similar to human p38 MAPK, is implicated in flagellar motility regulation of L. donovani.
[Mh] Termos MeSH primário: Flagelos/efeitos dos fármacos
Imidazóis/farmacologia
Leishmania donovani/efeitos dos fármacos
Leishmania donovani/fisiologia
Inibidores de Proteínas Quinases/farmacologia
Proteínas Quinases p38 Ativadas por Mitógeno/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Anisomicina/farmacologia
Antracenos/farmacologia
Flagelos/fisiologia
Flavonoides/farmacologia
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Sistema de Sinalização das MAP Quinases/fisiologia
Microscopia de Vídeo
Movimento/efeitos dos fármacos
Movimento/fisiologia
Proteínas de Protozoários/antagonistas & inibidores
Proteínas de Protozoários/fisiologia
Proteínas Quinases p38 Ativadas por Mitógeno/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one); 0 (Anthracenes); 0 (Flavonoids); 0 (Imidazoles); 0 (Protein Kinase Inhibitors); 0 (Protozoan Proteins); 1TW30Y2766 (pyrazolanthrone); 6C74YM2NGI (Anisomycin); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases); GX3Y2V80CV (2-(4-nitrophenyl)-4-(4-fluorophenyl)-5-(4-pyridinyl)-1H-imidazole)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170930
[St] Status:MEDLINE


  5 / 5538 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[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


  6 / 5538 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28887384
[Au] Autor:Kusuyama J; Ohnishi T; Bandow K; Amir MS; Shima K; Semba I; Matsuguchi T
[Ad] Endereço:Department of Oral Biochemistry, Field of Developmental Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, 8-35-1 Sakuragaoka, Kagoshima 890-8544, Japan.
[Ti] Título:Constitutive activation of p46JNK2 is indispensable for C/EBPδ induction in the initial stage of adipogenic differentiation.
[So] Source:Biochem J;474(20):3421-3437, 2017 Oct 05.
[Is] ISSN:1470-8728
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Adipogenic differentiation plays a vital role in energy homeostasis and endocrine system. Several transcription factors, including peroxisome proliferator-activated receptor gamma 2 and CCAAT-enhancer-binding protein (C/EBP) α, ß, and δ, are important for the process, whereas the stage-specific intracellular signal transduction regulating the onset of adipogenesis remains enigmatic. Here, we explored the functional role of c- N-terminal kinases (JNKs) in adipogenic differentiation using differentiation models of 3T3-L1 cells and primary adipo-progenitor cells. JNK inactivation with either a pharmacological inhibitor or JNK2-specific siRNA suppressed adipogenic differentiation, characterized by decreased lipid droplet appearance and the down-regulation of , ( ), , and expressions. Conversely, increased adipogenesis was observed by the inducible overexpression of p46JNK2 (JNK2-1), whereas it was not observed by that of p54JNK2 (JNK2-2), indicating a distinct role of p46JNK2. The essential role of JNK appears restricted to the early stage of adipogenic differentiation, as JNK inhibition in the later stages did not influence adipogenesis. Indeed, JNK phosphorylation was significantly induced at the onset of adipogenic differentiation. As for the transcription factors involved in early adipogenesis, JNK inactivation significantly inhibited the induction of , but not , during the initial stage of adipogenic differentiation. JNK activation increased mRNA and protein expression through the induction and phosphorylation of activating transcription factor 2 (ATF2) that binds to a responsive element within the gene promoter region. Taken together, these data indicate that constitutive JNK activity is specifically required for the initial stage differentiation events of adipocytes.
[Mh] Termos MeSH primário: Adipogenia/fisiologia
Proteína delta de Ligação ao Facilitador CCAAT/biossíntese
Diferenciação Celular/fisiologia
Proteína Quinase 9 Ativada por Mitógeno/metabolismo
[Mh] Termos MeSH secundário: Células 3T3-L1
Adipócitos/efeitos dos fármacos
Adipócitos/metabolismo
Adipogenia/efeitos dos fármacos
Animais
Antracenos/farmacologia
Diferenciação Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Ativação Enzimática/efeitos dos fármacos
Ativação Enzimática/fisiologia
Camundongos
Camundongos Endogâmicos C57BL
Proteína Quinase 9 Ativada por Mitógeno/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anthracenes); 142662-43-9 (CCAAT-Enhancer-Binding Protein-delta); 1TW30Y2766 (pyrazolanthrone); EC 2.7.1.24 (Mitogen-Activated Protein Kinase 9)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171012
[Lr] Data última revisão:
171012
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170910
[St] Status:MEDLINE
[do] DOI:10.1042/BCJ20170332


  7 / 5538 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28859160
[Au] Autor:Wang Y; Liu Y; Fan Z; Liu D; Wang F; Zhou Y
[Ad] Endereço:Department of Prosthodontics, Peking University School and Hospital of Stomatology, Beijing, China.
[Ti] Título:IGFBP2 enhances adipogenic differentiation potentials of mesenchymal stem cells from Wharton's jelly of the umbilical cord via JNK and Akt signaling pathways.
[So] Source:PLoS One;12(8):e0184182, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mesenchymal stem cell (MSC)-mediated tissue engineering represents a promising strategy to address adipose tissue defects. MSCs derived from Wharton's jelly of the umbilical cord (WJCMSCs) may serve as an ideal source for adipose tissue engineering due to their abundance, safety profile, and accessibility. How to activate the directed differentiation potentials of WJCMSCs is the core point for their clinical applications. A thorough investigation of mechanisms involved in WJCMSC adipogenic differentiation is necessary to support their application in adipose tissue engineering and address shortcomings. Previous study showed, compared with periodontal ligament stem cells (PDLSCs), WJCMSCs had a weakened adipogenic differentiation potentials and lower expression of insulin-like growth factor binding protein 2 (IGFBP2). IGFBP2 may be involved in the adipogenesis of MSCs. Generally, IGFBP2 is involved in regulating biological activity of insulin-like growth factors, however, its functions in human MSCs are unclear. Here, we found IGFBP2 expression was upregulated upon adipogenic induction, and that IGFBP2 enhanced adipogenic differentiation of WJCMSCs and BMSCs. Moreover, IGFBP2 increased phosphorylation of c-Jun N-terminal kinase (p-JNK) and p-Akt, and activated JNK or Akt signaling significantly promoted adipogenic differentiation of MSCs. Furthermore, inhibitor-mediated blockage of either JNK or Akt signaling dramatically reduced IGFBP2-mediated adipogenic differentiation. And the JNK inhibitor, SP600125 markedly blocked IGFBP2-mediated Akt activation. Moreover, IGFBP2 was negatively regulated by BCOR, which inhibited adipogenic differentiation of WJCMSCs. Overall, our results reveal a new function of IGFBP2, providing a novel insight into the mechanism of adipogenic differentiation and identifying a potential target mediator for improving adipose tissue engineering based on WJCMSCs.
[Mh] Termos MeSH primário: Diferenciação Celular/genética
Proteína 3 de Ligação a Fator de Crescimento Semelhante à Insulina/genética
Células Mesenquimais Estromais/citologia
Geleia de Wharton/citologia
[Mh] Termos MeSH secundário: Adipogenia/genética
Tecido Adiposo/citologia
Tecido Adiposo/crescimento & desenvolvimento
Antracenos/farmacologia
Seres Humanos
Sistema de Sinalização das MAP Quinases/genética
Osteogênese/genética
Proteínas Proto-Oncogênicas c-akt/genética
Transdução de Sinais/efeitos dos fármacos
Engenharia Tecidual
Cordão Umbilical/citologia
Geleia de Wharton/crescimento & desenvolvimento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anthracenes); 0 (IGFBP3 protein, human); 0 (Insulin-Like Growth Factor Binding Protein 3); 1TW30Y2766 (pyrazolanthrone); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171011
[Lr] Data última revisão:
171011
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170901
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184182


  8 / 5538 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28835457
[Au] Autor:Roewe J; Higer M; Riehl DR; Gericke A; Radsak MP; Bosmann M
[Ad] Endereço:Center for Thrombosis and Hemostasis, University Medical Center, Johannes Gutenberg University Mainz, 55131 Mainz, Germany.
[Ti] Título:Neuroendocrine Modulation of IL-27 in Macrophages.
[So] Source:J Immunol;199(7):2503-2514, 2017 Oct 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Heterodimeric IL-27 (p28/EBV-induced gene 3) is an important member of the IL-6/IL-12 cytokine family. IL-27 is predominantly synthesized by mononuclear phagocytes and exerts immunoregulatory functional activities on lymphocytic and nonlymphocytic cells during infection, autoimmunity or neoplasms. There is a great body of evidence on the bidirectional interplay between the autonomic nervous system and immune responses during inflammatory disorders, but so far IL-27 has not been defined as a part of these multifaceted neuroendocrine networks. In this study, we describe the role of catecholamines (as mediators of the sympathetic nervous system) related to IL-27 production in primary mouse macrophages. Noradrenaline and adrenaline dose-dependently suppressed the release of IL-27p28 in LPS/TLR4-activated macrophages, which was independent of α adrenoceptors. Instead, ß adrenoceptor activation was responsible for mediating gene silencing of IL-27p28 and EBV-induced gene 3. The ß adrenoceptor agonists formoterol and salbutamol mediated suppression of IL-27p28 production, when triggered by zymosan/TLR2, LPS/TLR4, or R848/TLR7/8 activation, but selectively spared the polyinosinic-polycytidylic acid/TLR3 pathway. Mechanistically, ß adrenergic signaling reinforced an autocrine feedback loop of macrophage-derived IL-10 and this synergized with inhibition of the JNK pathway for limiting IL-27p28. The JNK inhibitors SP600125 and AEG3482 strongly decreased intracellular IL-27p28 in F4/80 CD11b macrophages. In endotoxic shock of C57BL/6J mice, pharmacologic activation of ß adrenoceptors improved the severity of shock, including hypothermia and decreased circulating IL-27p28. Conversely, IL-27p28 was 2.7-fold increased by removal of the catecholamine-producing adrenal glands prior to endotoxic shock. These data suggest a novel role of the sympathetic neuroendocrine system for the modulation of IL-27-dependent acute inflammation.
[Mh] Termos MeSH primário: Epinefrina/farmacologia
Interleucinas/imunologia
Interleucinas/metabolismo
Macrófagos/efeitos dos fármacos
Macrófagos/imunologia
Norepinefrina/farmacologia
[Mh] Termos MeSH secundário: Albuterol/farmacologia
Animais
Antracenos/farmacologia
Células Cultivadas
Fumarato de Formoterol/farmacologia
Inflamação
Interleucina-10/biossíntese
Interleucina-10/imunologia
Interleucinas/sangue
Interleucinas/genética
Lipopolissacarídeos/farmacologia
Ativação de Macrófagos/efeitos dos fármacos
Camundongos
Camundongos Endogâmicos C57BL
Poli I-C/metabolismo
Receptores Adrenérgicos/efeitos dos fármacos
Choque Séptico
Transdução de Sinais/efeitos dos fármacos
Sulfonamidas/farmacologia
Sistema Nervoso Simpático/imunologia
Sistema Nervoso Simpático/fisiologia
Tiadiazóis/farmacologia
Receptor 3 Toll-Like/metabolismo
Zimosan/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AEG 3482); 0 (Anthracenes); 0 (Il27 protein, mouse); 0 (Interleukins); 0 (Lipopolysaccharides); 0 (Receptors, Adrenergic); 0 (Sulfonamides); 0 (Thiadiazoles); 0 (Toll-Like Receptor 3); 130068-27-8 (Interleukin-10); 1TW30Y2766 (pyrazolanthrone); 9010-72-4 (Zymosan); O84C90HH2L (Poly I-C); QF8SVZ843E (Albuterol); W34SHF8J2K (Formoterol Fumarate); X4W3ENH1CV (Norepinephrine); YKH834O4BH (Epinephrine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170825
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700687


  9 / 5538 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28733031
[Au] Autor:Kim JS; Kim EJ; Kim HS; Kurie JM; Ahn YH
[Ad] Endereço:Department of Molecular Medicine and Tissue Injury Defense Research Center, College of Medicine, Ewha Womans University, Seoul 07985, South Korea.
[Ti] Título:MKK4 activates non-canonical NFκB signaling by promoting NFκB2-p100 processing.
[So] Source:Biochem Biophys Res Commun;491(2):337-342, 2017 Sep 16.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The NFκB family of transcription factors is crucial for innate or adaptive immunity, inflammation, and diseases including cancer. The two NFκB signaling pathways (canonical and non-canonical) differ from each other in extracellular signals, membrane receptors, signaling adaptors, and dimer subunits. The p52 (NFκB2) subunit, which participates in the non-canonical pathway, is generated by ubiquitin-mediated processing of the p100 precursor. Here, we found that NFκB2 processing and activation were mediated by mitogen-activated protein kinase kinase-4 (MKK4) and its substrate c-Jun N-terminal kinase (JNK). In MKK4-null mouse embryonic fibroblasts (MEFs), serum- and lymphotoxin ß receptor (LTßR) antibody-induced processing of p100 and nuclear translocation of p52 were found to be defective. Serum and LTßR antibody activated the MKK4-JNK signaling pathway, and SP600125, a JNK inhibitor, blocked p100 processing. Cellular senescence, one of the responses regulated by the non-canonical NFκB pathway, was observed more frequently in MKK4-null MEFs than in wildtype cells. These results suggest that the MKK4/JNK-dependent pathway regulates NFκB2 processing/activation and, through this mechanism, MKK4 and NFκB2 control cellular growth and senescence.
[Mh] Termos MeSH primário: Células Epiteliais/metabolismo
Fibroblastos/metabolismo
MAP Quinase Quinase 4/genética
Subunidade p52 de NF-kappa B/genética
[Mh] Termos MeSH secundário: Animais
Antracenos/farmacologia
Brônquios/citologia
Brônquios/metabolismo
Linhagem Celular
Linhagem Celular Tumoral
Proliferação Celular
Senescência Celular
Células Epiteliais/citologia
Fibroblastos/citologia
Regulação da Expressão Gênica
Seres Humanos
Receptor beta de Linfotoxina/genética
Receptor beta de Linfotoxina/metabolismo
MAP Quinase Quinase 4/antagonistas & inibidores
MAP Quinase Quinase 4/metabolismo
Camundongos
Subunidade p52 de NF-kappa B/metabolismo
Inibidores de Proteínas Quinases/farmacologia
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anthracenes); 0 (LTBR protein, human); 0 (Lymphotoxin beta Receptor); 0 (NF-kappa B p52 Subunit); 0 (NFKB2 protein, human); 0 (Protein Kinase Inhibitors); 1TW30Y2766 (pyrazolanthrone); EC 2.7.12.2 (MAP Kinase Kinase 4); EC 2.7.12.2 (MAP2K4 protein, human)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170723
[St] Status:MEDLINE


  10 / 5538 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28719204
[Au] Autor:Feng ZL; Zhang LL; Zheng YD; Liu QY; Liu JX; Feng L; Huang L; Zhang QW; Lu JJ; Lin LG
[Ad] Endereço:State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau , Avenida da Universidade, Taipa, Macao 999078, People's Republic of China.
[Ti] Título:Norditerpenoids and Dinorditerpenoids from the Seeds of Podocarpus nagi as Cytotoxic Agents and Autophagy Inducers.
[So] Source:J Nat Prod;80(7):2110-2117, 2017 Jul 28.
[Is] ISSN:1520-6025
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Nine new norditerpenoids and dinorditerpenoids, 2-oxonagilactone A (1), 7ß-hydroxynagilactone D (2), nagilactones K and L (3 and 4), 3ß-hydroxynagilactone L (5), 2ß-hydroxynagilactone L (6), 3-epi-15-hydroxynagilactone D (7), 1α-chloro-2ß,3ß,15-trihydroxynagilactone L (8), and 15-hydroxynagilactone L (9), were isolated from the seeds of Podocarpus nagi, along with eight known analogues. The structures of the new compounds were established based on detailed NMR and HRESIMS analysis, as well as from their ECD spectra. The absolute configuration of the known compound 1-deoxy-2α-hydroxynagilactone A (16) was confirmed by single-crystal X-ray diffraction. All of the isolates were tested for their cytotoxic activities against cancer cells. The results indicated that compounds 4 and 6, as well as several known compounds, displayed cytotoxicity against A2780 and HEY cancer cells. Among the new compounds, 2ß-hydroxynagilactone L (6) showed IC values of less than 2.5 µM against the two cell lines used. Furthermore, compound 6 induced autophagic flux in A2780 cells, as evidenced by an enhanced expression level of the autophagy marker phosphatidylethanolamine-modified microtubule-associated protein light-chain 3 (LC3-II) and increased mRFP-GFP-LC3 puncta. Also, compound 6 activated the c-Jun N-terminal kinase (JNK) pathway, while pretreatment with the JNK inhibitor SP600125 decreased compound 6-induced autophagy.
[Mh] Termos MeSH primário: Antineoplásicos Fitogênicos/isolamento & purificação
Antineoplásicos Fitogênicos/farmacologia
Diterpenos/isolamento & purificação
Diterpenos/farmacologia
Medicamentos de Ervas Chinesas/isolamento & purificação
Medicamentos de Ervas Chinesas/farmacologia
Sementes/química
[Mh] Termos MeSH secundário: Antracenos/química
Antineoplásicos Fitogênicos/química
Autofagia/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Citotoxinas
Diterpenos/química
Ensaios de Seleção de Medicamentos Antitumorais
Medicamentos de Ervas Chinesas/química
Seres Humanos
Proteínas Quinases JNK Ativadas por Mitógeno/metabolismo
Estrutura Molecular
Ressonância Magnética Nuclear Biomolecular
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anthracenes); 0 (Antineoplastic Agents, Phytogenic); 0 (Cytotoxins); 0 (Diterpenes); 0 (Drugs, Chinese Herbal); 1TW30Y2766 (pyrazolanthrone); EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
[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:170719
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jnatprod.7b00347



página 1 de 554 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde