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[PMID]:29216642
[Au] Autor:Yang W; Huang J; Xiao B; Liu Y; Zhu Y; Wang F; Sun S
[Ti] Título:Taurine Protects Mouse Spermatocytes from Ionizing Radiation-Induced Damage Through Activation of Nrf2/HO-1 Signaling.
[So] Source:Cell Physiol Biochem;44(4):1629-1639, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: The increasing prevalence of ionizing radiation exposure has inevitably raised public concern over the potential detrimental effects of ionizing radiation on male reproductive system function. The detection of drug candidates to prevent reproductive system from damage caused by ionizing radiation is urgent. We aimed to investigate the protective role of taurine on the injury of mouse spermatocyte-derived cells (GC-2) subjected to ionizing radiation. METHODS: mouse spermatocytes (GC-2 cells) were exposed to ionizing radiation with or without treatment of Taurine. The effect of ionizing radiation and Taurine treatment on GC-2 cells were evaluated by cell viability assay (CCK8), cell cycle and apoptosis. The relative protein abundance change was determined by Western blotting. The siRNA was used to explore whether Nrf2 signaling was involved in the cytoprotection of Taurine. RESULTS: Taurine significantly inhibited the decrease of cell viability, percentage of apoptotic cells and cell cycle arrest induced by ionizing radiation. Western blot analysis showed that taurine significantly limited the ionizing radiation-induced down-regulation of CyclinB1 and CDK1, and suppressed activation of Fas/FasL system pathway. In addition, taurine treatment significantly increased the expression of Nrf2 and HO-1 in GC-2 cells exposed to ionizing radiation, two components in antioxidant pathway. The above cytoprotection of Taurine was blocked by siNrf2. CONCLUSION: Our results demonstrate that taurine has the potential to effectively protect GC-2 cells from ionizing radiation- triggered damage via upregulation of Nrf2/HO-1 signaling.
[Mh] Termos MeSH primário: Heme Oxigenase-1/metabolismo
Fator 2 Relacionado a NF-E2/metabolismo
Substâncias Protetoras/farmacologia
Radiação Ionizante
Transdução de Sinais/efeitos dos fármacos
Taurina/farmacologia
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Apoptose/efeitos da radiação
Proteína Quinase CDC2/metabolismo
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Pontos de Checagem do Ciclo Celular/efeitos da radiação
Linhagem Celular
Ciclina B1/metabolismo
Regulação para Baixo/efeitos dos fármacos
Proteína Ligante Fas/metabolismo
Masculino
Camundongos
Fator 2 Relacionado a NF-E2/antagonistas & inibidores
Fator 2 Relacionado a NF-E2/genética
Estresse Oxidativo/efeitos dos fármacos
Estresse Oxidativo/efeitos da radiação
Interferência de RNA
RNA Interferente Pequeno/metabolismo
Transdução de Sinais/efeitos da radiação
Espermatócitos/citologia
Espermatócitos/efeitos dos fármacos
Espermatócitos/metabolismo
Receptor fas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclin B1); 0 (Fas Ligand Protein); 0 (Fas protein, mouse); 0 (Fasl protein, mouse); 0 (NF-E2-Related Factor 2); 0 (Protective Agents); 0 (RNA, Small Interfering); 0 (fas Receptor); 1EQV5MLY3D (Taurine); EC 1.14.14.18 (Heme Oxygenase-1); EC 2.7.11.22 (CDC2 Protein Kinase)
[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:171208
[St] Status:MEDLINE
[do] DOI:10.1159/000485762


  2 / 11635 MEDLINE  
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[PMID]:29176759
[Au] Autor:Magalhães LMD; Viana A; de Jesus AC; Chiari E; Galvão L; Gomes JA; Gollob KJ; Dutra WO
[Ad] Endereço:Laboratório de Biologia das Interações Celulares, Departamento de Morfologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
[Ti] Título:Distinct Trypanosoma cruzi isolates induce activation and apoptosis of human neutrophils.
[So] Source:PLoS One;12(11):e0188083, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neutrophils are critical players in the first line of defense against pathogens and in the activation of subsequent cellular responses. We aimed to determine the effects of the interaction of Trypanosoma cruzi with human neutrophils, using isolates of the two major discrete type units (DTUs) associated with Chagas' disease in Latin America (clone Col1.7G2 and Y strain, DTU I and II, respectively). Thus, we used CFSE-stained trypomastigotes to measure neutrophil-T. cruzi interaction, neutrophil activation, cytokine expression and death, after infection with Col1.7G2 and Y strain. Our results show that the frequency of CFSE+ neutrophils, indicative of interaction, and CFSE intensity on a cell-per-cell basis were similar when comparing Col1.7G2 and Y strains. Interaction with T. cruzi increased neutrophil activation, as measured by CD282, CD284, TNF and IL-12 expression, although at different levels between the two strains. No change in IL-10 expression was observed after interaction of neutrophils with either strain. We observed that exposure to Y and Col1.7G2 caused marked neutrophil death. This was specific to neutrophils, since interaction of either strain with monocytes did not cause death. Our further analysis showed that neutrophil death was a result of apoptosis, which was associated with an upregulation of TNF-receptor, TNF and FasLigand, but not of Fas. Induction of TNF-associated neutrophil apoptosis by the different T. cruzi isolates may act as an effective common mechanism to decrease the host's immune response and favor parasite survival.
[Mh] Termos MeSH primário: Apoptose
Ativação de Neutrófilo
Neutrófilos/citologia
Trypanosoma cruzi/isolamento & purificação
[Mh] Termos MeSH secundário: Adulto
Antígenos CD/metabolismo
Sobrevivência Celular
Proteína Ligante Fas/metabolismo
Fluoresceínas/metabolismo
Seres Humanos
Interleucina-10/metabolismo
Interleucina-12/metabolismo
Neutrófilos/metabolismo
Receptores do Fator de Necrose Tumoral/metabolismo
Succinimidas/metabolismo
Receptor 2 Toll-Like/metabolismo
Receptor 4 Toll-Like/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
Adulto Jovem
Receptor fas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (5-(6)-carboxyfluorescein diacetate succinimidyl ester); 0 (Antigens, CD); 0 (FAS protein, human); 0 (Fas Ligand Protein); 0 (Fluoresceins); 0 (Receptors, Tumor Necrosis Factor); 0 (Succinimides); 0 (Toll-Like Receptor 2); 0 (Toll-Like Receptor 4); 0 (Tumor Necrosis Factor-alpha); 0 (fas Receptor); 130068-27-8 (Interleukin-10); 187348-17-0 (Interleukin-12)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171219
[Lr] Data última revisão:
171219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188083


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[PMID]:28929494
[Au] Autor:Pothoulakis C; Torre-Rojas M; Duran-Padilla MA; Gevorkian J; Zoras O; Chrysos E; Chalkiadakis G; Baritaki S
[Ad] Endereço:IBD Center, Division of Digestive Diseases, David Geffen School of Medicine at UCLA, Los Angeles, CA.
[Ti] Título:CRHR2/Ucn2 signaling is a novel regulator of miR-7/YY1/Fas circuitry contributing to reversal of colorectal cancer cell resistance to Fas-mediated apoptosis.
[So] Source:Int J Cancer;142(2):334-346, 2018 Jan 15.
[Is] ISSN:1097-0215
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Colorectal cancer (CRC) responds poorly to immuno-mediated cytotoxicity. Underexpression of corticotropin-releasing-hormone-receptor-2 (CRHR2) in CRC, promotes tumor survival, growth and Epithelial to Mesenchymal Transition (EMT), in vitro and in vivo. We explored the role of CRHR2 downregulation in CRC cell resistance to Fas/FasL-mediated apoptosis and the underlying molecular mechanism. CRC cell sensitivity to CH11-induced apoptosis was compared between Urocortin-2 (Ucn2)-stimulated parental and CRHR2-overexpressing CRC cell lines and targets of CRHR2/Ucn2 signaling were identified through in vitro and ex vivo analyses. Induced CRHR2/Ucn2 signaling in SW620 and DLD1 cells increased specifically their sensitivity to CH11-mediated apoptosis, via Fas mRNA and protein upregulation. CRC compared to control tissues had reduced Fas expression that was associated with lost CRHR2 mRNA, poor tumor differentiation and high risk for distant metastasis. YY1 silencing increased Fas promoter activity in SW620 and re-sensitized them to CH11-apoptosis, thus suggesting YY1 as a putative transcriptional repressor of Fas in CRC. An inverse correlation between Fas and YY1 expression was confirmed in CRC tissue arrays, while elevated YY1 mRNA was clinically relevant with advanced CRC grade and higher risk for distant metastasis. CRHR2/Ucn2 signaling downregulated specifically YY1 expression through miR-7 elevation, while miR-7 modulation in miR-7 SW620-CRHR2+ and miR-7 HCT116 cells, had opposite effects on YY1 and Fas expressions and cell sensitivity to CH11-killing. CRHR2/Ucn2 signaling is a negative regulator of CRC cell resistance to Fas/FasL-apoptosis via targeting the miR-7/YY1/Fas circuitry. CRHR2 restoration might prove effective in managing CRC response to immune-mediated apoptotic stimuli.
[Mh] Termos MeSH primário: Apoptose
Neoplasias Colorretais/patologia
Hormônio Liberador da Corticotropina/metabolismo
MicroRNAs/genética
Receptores de Hormônio Liberador da Corticotropina/metabolismo
Urocortinas/metabolismo
Fator de Transcrição YY1/metabolismo
Receptor fas/metabolismo
[Mh] Termos MeSH secundário: Proliferação Celular
Neoplasias Colorretais/genética
Neoplasias Colorretais/metabolismo
Hormônio Liberador da Corticotropina/genética
Transição Epitelial-Mesenquimal
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Receptores de Hormônio Liberador da Corticotropina/genética
Transdução de Sinais
Células Tumorais Cultivadas
Urocortinas/genética
Fator de Transcrição YY1/genética
Receptor fas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CRF receptor type 2); 0 (FAS protein, human); 0 (MIRN7 microRNA, human); 0 (MicroRNAs); 0 (Receptors, Corticotropin-Releasing Hormone); 0 (UCN2 protein, human); 0 (Urocortins); 0 (YY1 Transcription Factor); 0 (YY1 protein, human); 0 (fas Receptor); 9015-71-8 (Corticotropin-Releasing Hormone)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171214
[Lr] Data última revisão:
171214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170921
[St] Status:MEDLINE
[do] DOI:10.1002/ijc.31064


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[PMID]:29187439
[Au] Autor:Werner JM; Kuhl S; Stavrinou P; Röhn G; Krischek B; Blau T; Goldbrunner R; Timmer M
[Ad] Endereço:Department of General Neurosurgery, Center for Neurosurgery, University Hospital Cologne, Cologne, Germany.
[Ti] Título:Expression of FAS-L Differs from Primary to Relapsed Low-grade Gliomas and Predicts Progression-free Survival.
[So] Source:Anticancer Res;37(12):6639-6648, 2017 12.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: The tumor necrosis factor FAS is overexpressed in high-grade gliomas (HGG). Only little is known about FAS or FAS ligand (FAS-L) in low-grade gliomas (LGG). We explored FAS/FAS-L expression in LGG, focusing on differences in primary and relapsed LGG and on its prognostic value. PATIENTS AND METHODS: A total of 133 glioma samples (73 LGG, 60 HGG) were collected. The LGG samples included 15 matched pairs of primary and relapsed tumors. RT-PCR was performed to measure FAS/FAS-L expression, using subunit A, flavoprotein variant (SDHA) as housekeeper. Clinical data included progression free- (PFS) and overall survival (OS). RESULTS: LGG showed significantly lower FAS but higher FAS-L expression than HGG. The FAS-L expression was higher in primary compared to relapsed LGG and had a positive prognostic value concerning PFS (median 45.20 vs. 31.37 months). CONCLUSION: FAS-L could act as a prognostic marker and potential target in primary LGG.
[Mh] Termos MeSH primário: Neoplasias Encefálicas/genética
Proteína Ligante Fas/genética
Regulação Neoplásica da Expressão Gênica
Glioma/genética
[Mh] Termos MeSH secundário: Adulto
Neoplasias Encefálicas/metabolismo
Neoplasias Encefálicas/patologia
Progressão da Doença
Proteína Ligante Fas/metabolismo
Feminino
Glioma/patologia
Seres Humanos
Imuno-Histoquímica
Estimativa de Kaplan-Meier
Masculino
Meia-Idade
Gradação de Tumores
Prognóstico
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Receptor fas/genética
Receptor fas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fas Ligand Protein); 0 (fas Receptor)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171211
[Lr] Data última revisão:
171211
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE


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[PMID]:28796044
[Au] Autor:Chen J; Li JH; Zhao SJ; Wang DY; Zhang WZ; Liang WJ
[Ad] Endereço:aDepartment of Cardiovascular Medicine, Guangzhou Panyu Central Hospital, bPanyu District Cardiovascular Disease Research Institute of Guangzhou, Guangzhou, P.R. China.
[Ti] Título:Clinical significance of costimulatory molecules CD40/CD40L and CD134/CD134L in coronary heart disease: A case-control study.
[So] Source:Medicine (Baltimore);96(32):e7634, 2017 Aug.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The aim of the study was to evaluate the potential role of CD40/CD40 ligand (CD40L) and CD134/CD134 ligand (CD134L) in the development of coronary heart disease (CHD) via the performance of a case-control study.The research objects were 234 cases of CHD patients and 120 cases of well-matched normal controls. Following the separation of peripheral blood mononuclear cells (PBMCs), real-time quantitative PCR (qRT-PCR), Western blot, immunohistochemistry, and flow cytometry were applied for the detection of mRNA levels and expression levels of CD40/CD40L and CD134/CD134L; meanwhile, intercellular adhesion molecule-1 (ICAM-1) and Fas protein mRNA levels were detected using qRT-PCR.There was no statistical difference in the comparison of baseline characteristics between groups, indicating comparability between groups. qRT-PCR and Western blot analysis indicated that CD40/CD40L and CD134/CD134L mRNA and protein expression levels were all increased in the CHD group than those in the control group. Flow cytometry further confirmed the similar tendency. Meanwhile, ICAM-1 and Fas protein mRNA levels were elevated in the CHD group and positively correlated with the above parameters. Furthermore, CD40/CD40L expression rates were negatively correlated with gender and different types of CHD. Meanwhile, CD134/CD134L expressions were also higher in male patients, in patients with family history, previous history of hypertension, diabetes, and cerebrovascular diseases.CD40/CD40L and CD134/CD134L are increased and may have potential correlation with clinical pathological features of patients with CHD. Further in-depth exploration of costimulatory molecules for CHD guidance as well as intrinsic mechanisms are needed combined with in vivo and in vitro experiments.
[Mh] Termos MeSH primário: Antígenos CD40/biossíntese
Ligante de CD40/biossíntese
Doença das Coronárias/fisiopatologia
Ligante OX40/biossíntese
Receptores OX40/biossíntese
[Mh] Termos MeSH secundário: Adulto
Idoso
Estudos de Casos e Controles
Feminino
Citometria de Fluxo
Seres Humanos
Molécula 1 de Adesão Intercelular/biossíntese
Masculino
Meia-Idade
RNA Mensageiro
Reação em Cadeia da Polimerase em Tempo Real
Receptor fas/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (CD40 Antigens); 0 (FAS protein, human); 0 (OX40 Ligand); 0 (RNA, Messenger); 0 (Receptors, OX40); 0 (fas Receptor); 126547-89-5 (Intercellular Adhesion Molecule-1); 147205-72-9 (CD40 Ligand)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170811
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000007634


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[PMID]:28781259
[Au] Autor:Todosenko NM; Khaziakhmatova OG; Yurova KA; Malinina IP; Litvinova LS
[Ad] Endereço:Immanuel Kant Baltic Federal University.
[Ti] Título:[The influence of methylprednisolone on the ability of CD4+CD95+HLA-DR+ T-cells to produce proinflammatory medators in cultures of TCR-activated CD3+CD45RO+ T-lymphocytes from patients with rheumatoid arthritis].
[Ti] Título:Vliianie metilprednizolona na sposobnost' CD4+CD95+HLA-DR+ T-kletok v kul'turakh TCR-aktivirovannykh CD3+CD45RO+ T-limfotsitov bol'nykh revmatoidnym artritom produtsirovat' provospalitel'nye mediatory..
[So] Source:Biomed Khim;63(3):255-265, 2017 May.
[Is] ISSN:2310-6972
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:The effect of different concentrations of the glucocorticoid (GC) methylprednisolone (MP) on CD4+CD95+HLA-DR+ T-cells and their ability to produce proinflammatory mediators in cultures of TCR-stimulated CD3+CD45RO+ T-lymphocytes in the in vitro system was investigated. T cells were obtained from healthy donors and patients with rheumatoid arthritis (RA).Under conditions of TCR-activation, MP increased the number of CD4+HLA-DR+CD95+ cells in CD3+CD45RO+ cultures obtained from RA patients and did not change their content in the control group. In general, MP decreased production of proinflammatory factors (IFN-, IL-2, IL-17, IL-21 and TNF-) by TCR-activated CD3+CD45RO+ cells from healthy donors and RA, consistent with the overall immunosuppressive mechanism of GC action. The correlation between CD4+CD45RO+HLA-DR+CD95+ T-cell contents and parameters reflecting production of proinflammatory mediators (IL-17, IL-21 and TNF-) in RA patients indicates maintenance of the pro-inflammatory potential of this T-cell population exposed to GC action. We suggest that relative resistance of CD4+CD45RO+CD95+HLA-DR+ T-cells of RA patients to the suppressor effect of GC leads to maintenance and even enhancement in the functional capacities of autoreactive cells in the pathogenesis of RA.
[Mh] Termos MeSH primário: Artrite Reumatoide/imunologia
Linfócitos T CD4-Positivos/efeitos dos fármacos
Regulação da Expressão Gênica/efeitos dos fármacos
Glucocorticoides/farmacologia
Metilprednisolona/farmacologia
[Mh] Termos MeSH secundário: Adulto
Anticorpos/farmacologia
Artrite Reumatoide/patologia
Antígenos CD2/genética
Antígenos CD2/imunologia
Complexo CD3/genética
Complexo CD3/imunologia
Antígenos CD4/genética
Antígenos CD4/imunologia
Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD4-Positivos/patologia
Estudos de Casos e Controles
Feminino
Regulação da Expressão Gênica/imunologia
Antígenos HLA-DR/genética
Antígenos HLA-DR/imunologia
Seres Humanos
Interleucina-17/biossíntese
Interleucina-17/imunologia
Interleucina-2/biossíntese
Interleucina-2/imunologia
Interleucinas/biossíntese
Interleucinas/imunologia
Antígenos Comuns de Leucócito/genética
Antígenos Comuns de Leucócito/imunologia
Ativação Linfocitária
Masculino
Cultura Primária de Células
Transdução de Sinais
Fator de Necrose Tumoral alfa/biossíntese
Fator de Necrose Tumoral alfa/imunologia
Receptor fas/genética
Receptor fas/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies); 0 (CD2 Antigens); 0 (CD3 Complex); 0 (CD4 Antigens); 0 (FAS protein, human); 0 (Glucocorticoids); 0 (HLA-DR Antigens); 0 (Interleukin-17); 0 (Interleukin-2); 0 (Interleukins); 0 (Tumor Necrosis Factor-alpha); 0 (fas Receptor); 0 (interleukin-21); EC 3.1.3.48 (Leukocyte Common Antigens); X4W7ZR7023 (Methylprednisolone)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170808
[St] Status:MEDLINE
[do] DOI:10.18097/PBMC20176303255


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[PMID]:28727820
[Au] Autor:Fatehchand K; Santhanam R; Shen B; Erickson EL; Gautam S; Elavazhagan S; Mo X; Belay T; Tridandapani S; Butchar JP
[Ad] Endereço:Medical Scientist Training Program, The Ohio State University, Columbus, Ohio, United States of America.
[Ti] Título:Active hexose-correlated compound enhances extrinsic-pathway-mediated apoptosis of Acute Myeloid Leukemic cells.
[So] Source:PLoS One;12(7):e0181729, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Active Hexose Correlated Compound (AHCC) has been shown to have many immunostimulatory and anti-cancer activities in mice and in humans. As a natural product, AHCC has potential to create safer adjuvant therapies in cancer patients. Acute Myeloid Leukemia (AML) is the least curable and second-most common leukemia in adults. AML is especially terminal to those over 60 years old, where median survival is only 5 to 10 months, due to inability to receive intensive chemotherapy. Hence, the purpose of this study was to investigate the effects of AHCC on AML cells both in vitro and in vivo. Results showed that AHCC induced Caspase-3-dependent apoptosis in AML cell lines as well as in primary AML leukopheresis samples. Additionally, AHCC induced Caspase-8 cleavage as well as Fas and TRAIL upregulation, suggesting involvement of the extrinsic apoptotic pathway. In contrast, monocytes from healthy donors showed suppressed Caspase-3 cleavage and lower cell death. When tested in a murine engraftment model of AML, AHCC led to significantly increased survival time and decreased blast counts. These results uncover a mechanism by which AHCC leads to AML-cell specific death, and also lend support for the further investigation of AHCC as a potential adjuvant for the treatment of AML.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Apoptose/efeitos dos fármacos
Leucemia Mieloide Aguda/tratamento farmacológico
Polissacarídeos/farmacologia
[Mh] Termos MeSH secundário: Animais
Apoptose/fisiologia
Western Blotting
Caspase 3/metabolismo
Caspase 8/metabolismo
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Sobrevivência Celular/fisiologia
Relação Dose-Resposta a Droga
Avaliação Pré-Clínica de Medicamentos
Feminino
Leucemia Mieloide Aguda/metabolismo
Camundongos SCID
Monócitos/efeitos dos fármacos
Monócitos/metabolismo
Transplante de Neoplasias
Reação em Cadeia da Polimerase em Tempo Real
Ligante Indutor de Apoptose Relacionado a TNF/metabolismo
Receptor fas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (FAS protein, human); 0 (Polysaccharides); 0 (TNF-Related Apoptosis-Inducing Ligand); 0 (TNFSF10 protein, human); 0 (fas Receptor); EC 3.4.22.- (CASP3 protein, human); EC 3.4.22.- (CASP8 protein, human); EC 3.4.22.- (Caspase 3); EC 3.4.22.- (Caspase 8); S1W5KTD68Y (Active Hexose Correlated Compound)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170721
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0181729


  8 / 11635 MEDLINE  
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[PMID]:28711683
[Au] Autor:Veiga FMS; Graus-Nunes F; Rachid TL; Barreto AB; Mandarim-de-Lacerda CA; Souza-Mello V
[Ad] Endereço:Laboratory of Morphometry, Metabolism and Cardiovascular Disease, Biomedical Center, Institute of Biology, State University of Rio de Janeiro, Brazil.
[Ti] Título:Anti-obesogenic effects of WY14643 (PPAR-alpha agonist): Hepatic mitochondrial enhancement and suppressed lipogenic pathway in diet-induced obese mice.
[So] Source:Biochimie;140:106-116, 2017 Sep.
[Is] ISSN:1638-6183
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Non-alcoholic fatty liver disease (NAFLD) presents with growing prevalence worldwide, though its pharmacological treatment remains to be established. This study aimed to evaluate the effects of a PPAR-alpha agonist on liver tissue structure, ultrastructure, and metabolism, focusing on gene and protein expression of de novo lipogenesis and gluconeogenesis pathways, in diet-induced obese mice. Male C57BL/6 mice (three months old) received a control diet (C, 10% of lipids, n = 10) or a high-fat diet (HFD, 50% of lipids, n = 10) for ten weeks. These groups were subdivided to receive the treatment (n = 5 per group): C, C-alpha (PPAR-alpha agonist, 2.5 mg/kg/day mixed in the control diet), HFD and HFD-alpha group (PPAR-alpha agonist, 2.5 mg/kg/day mixed in the HFD). The effects were compared with biometrical, biochemical, molecular biology and transmission electron microscopy (TEM) analyses. HFD showed greater body mass (BM) and insulinemia than C, both of which were tackled by the treatment in the HFD-alpha group. Increased hepatic protein expression of glucose-6-phosphatase, CHREBP and gene expression of PEPCK in HFD points to increased gluconeogenesis. Treatment rescued these parameters in the HFD-alpha group, eliciting a reduced hepatic glucose output, confirmed by the smaller GLUT2 expression in HFD-alpha than in HFD. Conversely, favored de novo lipogenesis was found in the HFD group by the increased expression of PPAR-gamma, and its target gene SREBP-1, FAS and GK when compared to C. The treatment yielded a marked reduction in the expression of all lipogenic factors. TEM analyses showed a greater numerical density of mitochondria per area of tissue in treated than in untreated groups, suggesting an increase in beta-oxidation and the consequent NAFLD control. PPAR-alpha activation reduced BM and treated insulin resistance (IR) and NAFLD by increasing the number of mitochondria and reducing hepatic gluconeogenesis and de novo lipogenesis protein and gene expressions in a murine obesity model.
[Mh] Termos MeSH primário: Gorduras na Dieta/efeitos adversos
Fígado/metabolismo
Mitocôndrias Hepáticas/metabolismo
Obesidade/tratamento farmacológico
PPAR alfa/agonistas
Pirimidinas/farmacologia
[Mh] Termos MeSH secundário: Animais
Gorduras na Dieta/farmacologia
Regulação da Expressão Gênica/efeitos dos fármacos
Glucose-6-Fosfatase/biossíntese
Resistência à Insulina
Lipogênese/efeitos dos fármacos
Fígado/patologia
Masculino
Camundongos
Mitocôndrias Hepáticas/patologia
Hepatopatia Gordurosa não Alcoólica/induzido quimicamente
Hepatopatia Gordurosa não Alcoólica/tratamento farmacológico
Hepatopatia Gordurosa não Alcoólica/metabolismo
Hepatopatia Gordurosa não Alcoólica/patologia
Proteínas Nucleares/biossíntese
Obesidade/induzido quimicamente
Obesidade/metabolismo
Obesidade/patologia
PPAR alfa/metabolismo
PPAR gama/biossíntese
Fosfoenolpiruvato Carboxiquinase (ATP)/biossíntese
Proteína de Ligação a Elemento Regulador de Esterol 1/biossíntese
Fatores de Transcrição/biossíntese
Receptor fas/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dietary Fats); 0 (Fas protein, mouse); 0 (Mlxipl protein, mouse); 0 (Nuclear Proteins); 0 (PPAR alpha); 0 (PPAR gamma); 0 (Pyrimidines); 0 (Srebf1 protein, mouse); 0 (Sterol Regulatory Element Binding Protein 1); 0 (Transcription Factors); 0 (fas Receptor); 86C4MRT55A (pirinixic acid); EC 3.1.3.9 (Glucose-6-Phosphatase); EC 4.1.1.49 (Phosphoenolpyruvate Carboxykinase (ATP))
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170717
[St] Status:MEDLINE


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[PMID]:28698139
[Au] Autor:Zhang H; Zhou F; Pan Z; Bu X; Wang Y; Chen F
[Ad] Endereço:Department of Orthopedics, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, PR China.
[Ti] Título:11ß-hydroxysteroid dehydrogenases-2 decreases the apoptosis of MC3T3/MLO-Y4 cells induced by glucocorticoids.
[So] Source:Biochem Biophys Res Commun;490(4):1399-1406, 2017 Sep 02.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The aim of the present study was to confirm the role of 11ß-hydroxysteroid dehydrogenases type 2(11ß-HSD-2) in steroid induced osteonecrosis of the femoral head(SANFH). We cultured mouse bone-like cells (MLO-Y4) and mouse osteoblast-like cells (MC3T3-E1). After overexpressed 11ß-HSD-2 successfully, we induced cell apoptosis by dexamethasone (DXM). The level of cell apoptosis, the expression of Bcl-2 in MLO-Y4 cells and the expression of Fas and caspase8 in MC3T3-E1 cells were detected. Then, we constructed 11ß-HSD-2 siRNA plasmid and represented it on MLO-Y4/MC3T3-E1 Cells, to down-regulate the 11ß-HSD-2 expression. After that, we used dexamethasone to induce cell apoptosis. The level of cell apoptosis, the expression of Bcl-2 in MLO-Y4 cells and the expression of Fas and caspase8 in MC3T3-E1 cells were detected again. In the overexpression model of cells, we found that the amount of cell apoptosis, the expression of Fas and caspase8 in MC3T3-E1 cells are lower than that of control groups. The amount of cell apoptosis, the expression of Fas and caspase8 in MC3T3-E1 cells were more than before when we reduced the expression of 11ß-HSD-2. In our study, we concluded that 11ß-HSD-2 plays an important role in the development of bone or osteoblast cell apoptosis, and the decreased expression of 11ß-HSD-2 may aggravate steroid induced bone/osteoblast cell apoptosis.
[Mh] Termos MeSH primário: 11-beta-Hidroxiesteroide Desidrogenases/genética
Dexametasona/farmacologia
Glucocorticoides/farmacologia
Osteoblastos/efeitos dos fármacos
Osteócitos/efeitos dos fármacos
[Mh] Termos MeSH secundário: 11-beta-Hidroxiesteroide Desidrogenases/antagonistas & inibidores
11-beta-Hidroxiesteroide Desidrogenases/metabolismo
Animais
Apoptose/efeitos dos fármacos
Caspase 8/genética
Caspase 8/metabolismo
Diferenciação Celular/efeitos dos fármacos
Linhagem Celular
Regulação da Expressão Gênica
Camundongos
Osteoblastos/citologia
Osteoblastos/metabolismo
Osteócitos/citologia
Osteócitos/metabolismo
Proteínas Proto-Oncogênicas c-bcl-2/genética
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
RNA Interferente Pequeno/genética
RNA Interferente Pequeno/metabolismo
Transdução de Sinais
Receptor fas/genética
Receptor fas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fas protein, mouse); 0 (Glucocorticoids); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (RNA, Small Interfering); 0 (fas Receptor); 114100-40-2 (Bcl2 protein, mouse); 7S5I7G3JQL (Dexamethasone); EC 1.1.1.146 (11-beta-Hydroxysteroid Dehydrogenases); EC 3.4.22.- (Casp8 protein, mouse); EC 3.4.22.- (Caspase 8)
[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:170713
[St] Status:MEDLINE


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[PMID]:28687489
[Au] Autor:Hutami IR; Izawa T; Mino-Oka A; Shinohara T; Mori H; Iwasa A; Tanaka E
[Ad] Endereço:Department of Orthodontics and Dentofacial Orthopedics, Institute of Biomedical Sciences, Tokushima University Graduate School, 3-18-15 Kuramoto-cho, Tokushima 7708504, Japan.
[Ti] Título:Fas/S1P crosstalk via NF-κB activation in osteoclasts controls subchondral bone remodeling in murine TMJ arthritis.
[So] Source:Biochem Biophys Res Commun;490(4):1274-1281, 2017 Sep 02.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Enhanced turnover of subchondral trabecular bone is a hallmark of rheumatoid arthritis (RA) and it results from an imbalance between bone resorption and bone formation activities. To investigate the formation and activation of osteoclasts which mediate bone resorption, a Fas-deficient MRL/lpr mouse model which spontaneously develops autoimmune arthritis and exhibits decreased bone mass was studied. Various assays were performed on subchondral trabecular bone of the temporomandibular joint (TMJ) from MRL/lpr mice and MRL+/+ mice. Initially, greater osteoclast production was observed in vitro from bone marrow macrophages obtained from MRL/lpr mice due to enhanced phosphorylation of NF-κB, as well as Akt and MAPK, to receptor activator of nuclear factor-κB ligand (RANKL). Expression of sphingosine 1-phosphate receptor 1 (S1P ) was also significantly upregulated in the condylar cartilage. S1P was found to be required for S1P-induced migration of osteoclast precursor cells and downstream signaling via Rac1. When SN50, a synthetic NF-κB-inhibitory peptide, was applied to the MRL/lpr mice, subchondral trabecular bone loss was reduced and both production of osteoclastogenesis markers and sphingosine kinase (Sphk) 1/S1P signaling were reduced. Thus, the present results suggest that Fas/S1P signaling via activation of NF-κB in osteoclast precursor cells is a key factor in the pathogenesis of RA in the TMJ.
[Mh] Termos MeSH primário: Artrite Reumatoide/imunologia
Reabsorção Óssea/imunologia
NF-kappa B/imunologia
Osteoclastos/efeitos dos fármacos
Receptores de Lisoesfingolipídeo/imunologia
Articulação Temporomandibular/imunologia
Receptor fas/imunologia
[Mh] Termos MeSH secundário: Animais
Artrite Reumatoide/tratamento farmacológico
Artrite Reumatoide/genética
Artrite Reumatoide/patologia
Autoimunidade
Células da Medula Óssea/efeitos dos fármacos
Células da Medula Óssea/imunologia
Células da Medula Óssea/patologia
Reabsorção Óssea/genética
Reabsorção Óssea/patologia
Reabsorção Óssea/prevenção & controle
Diferenciação Celular
Modelos Animais de Doenças
Feminino
Regulação da Expressão Gênica
Lisofosfolipídeos/imunologia
Macrófagos/efeitos dos fármacos
Macrófagos/imunologia
Macrófagos/patologia
Camundongos
Camundongos Endogâmicos MRL lpr
Proteínas Quinases Ativadas por Mitógeno/genética
Proteínas Quinases Ativadas por Mitógeno/imunologia
NF-kappa B/antagonistas & inibidores
NF-kappa B/genética
Neuropeptídeos/genética
Neuropeptídeos/imunologia
Osteoclastos/imunologia
Osteoclastos/patologia
Osteogênese/efeitos dos fármacos
Osteogênese/imunologia
Peptídeos/farmacologia
Fosfotransferases (Aceptor do Grupo Álcool)/genética
Fosfotransferases (Aceptor do Grupo Álcool)/imunologia
Cultura Primária de Células
Proteínas Proto-Oncogênicas c-akt/genética
Proteínas Proto-Oncogênicas c-akt/imunologia
Ligante RANK/genética
Ligante RANK/imunologia
Receptores de Lisoesfingolipídeo/genética
Transdução de Sinais
Esfingosina/análogos & derivados
Esfingosina/imunologia
Articulação Temporomandibular/efeitos dos fármacos
Articulação Temporomandibular/patologia
Receptor fas/genética
Proteínas rac1 de Ligação ao GTP/genética
Proteínas rac1 de Ligação ao GTP/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fas protein, mouse); 0 (Lysophospholipids); 0 (NF-kappa B); 0 (Neuropeptides); 0 (Peptides); 0 (RANK Ligand); 0 (Rac1 protein, mouse); 0 (Receptors, Lysosphingolipid); 0 (SN50 peptide); 0 (TNFSF11 protein, human); 0 (fas Receptor); 26993-30-6 (sphingosine 1-phosphate); EC 2.7.1.- (Phosphotransferases (Alcohol Group Acceptor)); EC 2.7.1.- (sphingosine kinase); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); EC 3.6.5.2 (rac1 GTP-Binding Protein); NGZ37HRE42 (Sphingosine)
[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:170709
[St] Status:MEDLINE



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