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

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

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

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

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

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

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

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

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

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

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			PalavrasDescritor de assuntoDescritor de assunto primárioLimitesAutorPalavras do títuloPalavras do resumoIdiomaPaís de publicaçãoNome de substânciaNome de pessoa como assuntoRevistaAssunto de RevistaISSNTipo de publicaçãoIdentificador únicoMês de entradaAno de publicaçãoTexto completoAtualização por classeCategoria DeCSCategoria DeCS explodidaCategoria CID-10SubSetsPais de AfiliaçãoAfiliaçãoAfiliação 2
2	and or and not		PalavrasDescritor de assuntoDescritor de assunto primárioLimitesAutorPalavras do títuloPalavras do resumoIdiomaPaís de publicaçãoNome de substânciaNome de pessoa como assuntoRevistaAssunto de RevistaISSNTipo de publicaçãoIdentificador únicoMês de entradaAno de publicaçãoTexto completoAtualização por classeCategoria DeCSCategoria DeCS explodidaCategoria CID-10SubSetsPais de AfiliaçãoAfiliaçãoAfiliação 2
3	and or and not		PalavrasDescritor de assuntoDescritor de assunto primárioLimitesAutorPalavras do títuloPalavras do resumoIdiomaPaís de publicaçãoNome de substânciaNome de pessoa como assuntoRevistaAssunto de RevistaISSNTipo de publicaçãoIdentificador únicoMês de entradaAno de publicaçãoTexto completoAtualização por classeCategoria DeCSCategoria DeCS explodidaCategoria CID-10SubSetsPais de AfiliaçãoAfiliaçãoAfiliação 2

Search engine: iAH v2.6 powered by WWWISIS

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