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[PMID]:28746790
[Au] Autor:Zhang J; Li Z; Liu L; Wang Q; Li S; Chen D; Hu Z; Yu T; Ding J; Li J; Yao M; Huang S; Zhao Y; He X
[Ad] Endereço:Fudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University, Shanghai, China.
[Ti] Título:Long noncoding RNA TSLNC8 is a tumor suppressor that inactivates the interleukin-6/STAT3 signaling pathway.
[So] Source:Hepatology;67(1):171-187, 2018 01.
[Is] ISSN:1527-3350
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Long noncoding RNAs can serve as oncogenes or tumor suppressors in human cancer; however, their biological functions and underlying mechanism in hepatocarcinogenesis are largely unknown. Here, we report a novel tumor suppressor long noncoding RNA on chromosome 8p12 (termed TSLNC8) that is frequently deleted and down-regulated in hepatocellular carcinoma (HCC) tissues. The loss of TSLNC8 is highly associated with the malignant features of HCC and serves as a prognostic indicator for HCC patients. TSLNC8 significantly suppresses the proliferation and metastasis of HCC cells in vitro and in vivo. TSLNC8 exerts its tumor suppressive activity by competitively interacting with transketolase and signal transducer and activator of transcription 3 (STAT3) and modulating the STAT3-Tyr705 and STAT3-Ser727 phosphorylation levels and STAT3 transcriptional activity, thus resulting in inactivation of the interleukin-6-STAT3 signaling pathway in HCC cells. CONCLUSION: TSLNC8 is a promising prognostic predictor for patients with HCC, and the TSLNC8-transketolase-STAT3 axis is a potential therapeutic target for HCC treatment. (Hepatology 2018;67:171-187).
[Mh] Termos MeSH primário: Biomarcadores Tumorais/genética
Carcinoma Hepatocelular/patologia
Interleucina-6/metabolismo
Neoplasias Hepáticas/patologia
RNA Longo não Codificante/metabolismo
Fator de Transcrição STAT3/metabolismo
[Mh] Termos MeSH secundário: Análise de Variância
Biópsia por Agulha
Carcinoma Hepatocelular/metabolismo
Linhagem Celular Tumoral
Receptor gp130 de Citocina/metabolismo
Regulação para Baixo
Genes Supressores de Tumor
Seres Humanos
Imuno-Histoquímica
Neoplasias Hepáticas/metabolismo
Fosforilação
Projetos Piloto
Prognóstico
Modelos de Riscos Proporcionais
RNA Longo não Codificante/genética
Curva ROC
Fator de Transcrição STAT3/genética
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (IL6ST protein, human); 0 (Interleukin-6); 0 (RNA, Long Noncoding); 0 (STAT3 Transcription Factor); 133483-10-0 (Cytokine Receptor gp130)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180123
[Lr] Data última revisão:
180123
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.1002/hep.29405


  2 / 1424 MEDLINE  
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[PMID]:28886093
[Au] Autor:Peláez-García A; Yébenes L; Berjón A; Angulo A; Zamora P; Sánchez-Méndez JI; Espinosa E; Redondo A; Heredia-Soto V; Mendiola M; Feliú J; Hardisson D
[Ad] Endereço:Department of Pathology, Hospital Universitario La Paz, IdiPAZ, Madrid, Spain.
[Ti] Título:Comparison of risk classification between EndoPredict and MammaPrint in ER-positive/HER2-negative primary invasive breast cancer.
[So] Source:PLoS One;12(9):e0183452, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: To compare the concordance in risk classification between the EndoPredict and the MammaPrint scores obtained for the same cancer samples on 40 estrogen-receptor positive/HER2-negative breast carcinomas. METHODS: Formalin-fixed, paraffin-embedded invasive breast carcinoma tissues that were previously analyzed with MammaPrint as part of routine care of the patients, and were classified as high-risk (20 patients) and low-risk (20 patients), were selected to be analyzed by the EndoPredict assay, a second generation gene expression test that combines expression of 8 genes (EP score) with two clinicopathological variables (tumor size and nodal status, EPclin score). RESULTS: The EP score classified 15 patients as low-risk and 25 patients as high-risk. EPclin re-classified 5 of the 25 EP high-risk patients into low-risk, resulting in a total of 20 high-risk and 20 low-risk tumors. EP score and MammaPrint score were significantly correlated (p = 0.008). Twelve of 20 samples classified as low-risk by MammaPrint were also low-risk by EP score (60%). 17 of 20 MammaPrint high-risk tumors were also high-risk by EP score. The overall concordance between EP score and MammaPrint was 72.5% (κ = 0.45, (95% CI, 0.182 to 0.718)). EPclin score also correlated with MammaPrint results (p = 0.004). Discrepancies between both tests occurred in 10 cases: 5 MammaPrint low-risk patients were classified as EPclin high-risk and 5 high-risk MammaPrint were classified as low-risk by EPclin and overall concordance of 75% (κ = 0.5, (95% CI, 0.232 to 0.768)). CONCLUSIONS: This pilot study demonstrates a limited concordance between MammaPrint and EndoPredict. Differences in results could be explained by the inclusion of different gene sets in each platform, the use of different methodology, and the inclusion of clinicopathological parameters, such as tumor size and nodal status, in the EndoPredict test.
[Mh] Termos MeSH primário: Neoplasias da Mama/metabolismo
Neoplasias da Mama/patologia
Receptor ErbB-2/metabolismo
Receptores Estrogênicos/metabolismo
[Mh] Termos MeSH secundário: Proteínas de Ligação ao Cálcio/metabolismo
Calmodulina/metabolismo
Proteínas de Transporte/metabolismo
Receptor gp130 de Citocina/metabolismo
Proteínas da Matriz Extracelular/metabolismo
Feminino
Glicoproteínas/metabolismo
Seres Humanos
Imuno-Histoquímica
Técnicas In Vitro
Proteínas Inibidoras de Apoptose/metabolismo
Peptídeos e Proteínas de Sinalização Intercelular/metabolismo
Antígeno Ki-67/metabolismo
Meia-Idade
Oxirredutases atuantes sobre Doadores de Grupo CH-CH/metabolismo
Proteínas/metabolismo
Receptores de Progesterona/metabolismo
Proteínas Ribossômicas/metabolismo
Enzimas de Conjugação de Ubiquitina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AZGP1 protein, human); 0 (BIRC5 protein, human); 0 (CALM2 protein, human); 0 (Calcium-Binding Proteins); 0 (Calmodulin); 0 (Carrier Proteins); 0 (Extracellular Matrix Proteins); 0 (Glycoproteins); 0 (IL6ST protein, human); 0 (Inhibitor of Apoptosis Proteins); 0 (Intercellular Signaling Peptides and Proteins); 0 (Ki-67 Antigen); 0 (Proteins); 0 (RPL37A protein, human); 0 (Receptors, Estrogen); 0 (Receptors, Progesterone); 0 (Ribosomal Proteins); 0 (STC2 protein, human); 0 (matrix Gla protein); 0 (ornithine decarboxylase antizyme); 133483-10-0 (Cytokine Receptor gp130); EC 1.3.- (Oxidoreductases Acting on CH-CH Group Donors); EC 1.3.1.21 (7-dehydrocholesterol reductase); EC 2.3.2.23 (UBE2C protein, human); EC 2.3.2.23 (Ubiquitin-Conjugating Enzymes); EC 2.7.10.1 (Receptor, ErbB-2)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170909
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0183452


  3 / 1424 MEDLINE  
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[PMID]:28878084
[Au] Autor:Chen D; Xiang Q; Nicholas J
[Ad] Endereço:Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
[Ti] Título:Human Herpesvirus 8 Interleukin-6 Interacts with Calnexin Cycle Components and Promotes Protein Folding.
[So] Source:J Virol;91(22), 2017 Nov 15.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Viral interleukin-6 (vIL-6) encoded by human herpesvirus 8 (HHV-8) is believed to contribute via mitogenic, survival, and angiogenic activities to HHV-8-associated Kaposi's sarcoma, primary effusion lymphoma (PEL), and multicentric Castleman's disease through autocrine or paracrine mechanisms during latency or productive replication. There is direct evidence that vIL-6 promotes latently infected PEL cell viability and proliferation and also viral productive replication in PEL and endothelial cells. These activities are mediated largely through endoplasmic reticulum (ER)-localized vIL-6, which can induce signal transduction via the gp130 signaling receptor, activating mitogen-activated protein kinase and signal transducer and activator of transcription signaling, and interactions of vIL-6 with the ER membrane protein vitamin K epoxide reductase complex subunit 1 variant 2 (VKORC1v2). The latter functional axis involves suppression of proapoptotic lysosomal protein cathepsin D by promotion of the ER-associated degradation of ER-transiting, preproteolytically processed procathepsin D. Other interactions of VKORC1v2 and activities of vIL-6 via the receptor have not been reported. We show here that both vIL-6 and VKORC1v2 interact with calnexin cycle proteins UDP-glucose:glycoprotein glucosyltransferase 1 (UGGT1), which catalyzes monoglucosylation of N-glycans, and oppositely acting glucosidase II (GlucII), and that vIL-6 can promote protein folding. This activity was found to require VKORC1v2 and UGGT1, to involve vIL-6 associations with VKORC1v2, UGGT1, and GlucII, and to operate in the context of productively infected cells. These findings document new VKORC1v2-associated interactions and activities of vIL-6, revealing novel mechanisms of vIL-6 function within the ER compartment. HHV-8 vIL-6 prosurvival (latent) and proreplication functions are mediated from the ER compartment through both gp130 receptor-mediated signal transduction and interaction of vIL-6 with the ER membrane protein VKORC1v2. This report identifies interactions of vIL-6 and VKORC1v2 with calnexin cycle enzymes GlucII and UGGT1, which are involved in glycan processing and nascent protein folding. The presented data show that vIL-6 and VKORC1v2 can cocomplex with GlucII and UGGT1, that vIL-6 promotes protein folding, and that VKORC1v2, UGGT1, and vIL-6 interactions with GlucII and UGGT1 are important for the profolding activity of vIL-6, which can be detected in the context of infected cells. This newly identified ER activity of vIL-6 involving VKORC1v2 may promote viral latency (in PEL cells) and productive replication by limiting the damaging effects of unfolded protein response signaling in addition to enhancing viral protein folding. This is the first report of such a function for a cytokine.
[Mh] Termos MeSH primário: Retículo Endoplasmático/metabolismo
Glucosiltransferases/metabolismo
Herpesvirus Humano 8/metabolismo
Interleucina-6/metabolismo
Sarcoma de Kaposi/metabolismo
Proteínas Virais/metabolismo
Vitamina K Epóxido Redutases/metabolismo
[Mh] Termos MeSH secundário: Receptor gp130 de Citocina/genética
Receptor gp130 de Citocina/metabolismo
Retículo Endoplasmático/genética
Retículo Endoplasmático/virologia
Glucosiltransferases/genética
Células HEK293
Herpesvirus Humano 8/genética
Seres Humanos
Interleucina-6/genética
Dobramento de Proteína
Sarcoma de Kaposi/genética
Proteínas Virais/genética
Vitamina K Epóxido Redutases/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-6); 0 (Viral Proteins); 133483-10-0 (Cytokine Receptor gp130); EC 1.17.4.4 (VKORC1 protein, human); EC 1.17.4.4 (Vitamin K Epoxide Reductases); EC 2.4.1.- (Glucosyltransferases); EC 2.4.1.- (UGGT1 protein, human)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170908
[St] Status:MEDLINE


  4 / 1424 MEDLINE  
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[PMID]:28675418
[Au] Autor:Rose-John S
[Ad] Endereço:Institute of Biochemistry, University of Kiel, Germany.
[Ti] Título:The Soluble Interleukin 6 Receptor: Advanced Therapeutic Options in Inflammation.
[So] Source:Clin Pharmacol Ther;102(4):591-598, 2017 Oct.
[Is] ISSN:1532-6535
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Interleukin (IL)-6 binds to IL-6R and the complex of IL-6 and IL-6R associates with the receptor subunit gp130, which initiates signaling. gp130 is expressed on all cells. IL-6R is cleaved by the ADAM17, generating a soluble IL-6R (sIL-6R). The sIL-6R binds IL-6 and the complex of IL-6 and sIL-6R binds to gp130 even on cells that do not express IL-6R. This process, which has been called IL-6 trans-signaling, increases the spectrum of target cells for IL-6. We generated a protein, sgp130Fc, which inhibits IL-6 trans-signaling without affecting IL-6 classic signaling. Using the sgp130Fc protein we demonstrated that IL-6 classic signaling is antiinflammatory and protective, whereas IL-6 trans-signaling is proinflammatory. Blocking IL-6 trans-signaling does not compromise the defense of the body against bacterial infections. We suggest that sgp130Fc is a superior agent as compared to IL-6 or IL-6R antibodies to block IL-6. The sgp130Fc protein is in phase II clinical trials.
[Mh] Termos MeSH primário: Inflamação/tratamento farmacológico
Interleucina-6/metabolismo
Receptores de Interleucina-6/metabolismo
Proteínas Recombinantes de Fusão/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Receptor gp130 de Citocina/metabolismo
Desenho de Drogas
Seres Humanos
Inflamação/imunologia
Inflamação/patologia
Interleucina-6/imunologia
Receptores de Interleucina-6/imunologia
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Interleukin-6); 0 (Receptors, Interleukin-6); 0 (Recombinant Fusion Proteins); 0 (Sgp130Fc protein); 133483-10-0 (Cytokine Receptor gp130)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170705
[St] Status:MEDLINE
[do] DOI:10.1002/cpt.782


  5 / 1424 MEDLINE  
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[PMID]:28672024
[Au] Autor:Xiao H; Bid HK; Chen X; Wu X; Wei J; Bian Y; Zhao C; Li H; Li C; Lin J
[Ad] Endereço:Center for Childhood Cancer and Blood Diseases, The Research Institute at Nationwide Children's Hospital, Columbus, Ohio, United States of America.
[Ti] Título:Repositioning Bazedoxifene as a novel IL-6/GP130 signaling antagonist for human rhabdomyosarcoma therapy.
[So] Source:PLoS One;12(7):e0180297, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Interleukins-6 (IL-6)/GP130 signaling pathway represents a promising target for cancer therapy due to its critical role in survival and progression of multiple types of cancer. We have identified Bazedoxifene, a Food and Drug Administration (FDA)-approved drug used for the prevention of postmenopausal osteoporosis, with novel function as inhibitor of IL-6/GP130 interaction. In this study, we investigate the effect of Bazedoxifene in rhabdomyosarcoma and evaluate whether inhibiting IL-6/GP130 signaling is an effective therapeutic strategy for rhabdomyosarcoma. The inhibitory effect of Bazedoxifene was assessed in rhabdomyosarcoma cell lines in vitro and RH30 xenograft model was used to further examine the suppressive efficacy of Bazedoxifene on tumor growth in vivo. Rhabdomyosarcoma cells showed their sensitivity to GP130 inhibition using gene knockdown or neutralized antibody, suggesting IL-6/GP130 as therapeutic target in rhabdomyosarcoma cells. Bazedoxifene decreased the signal transducer and activator of transcription3 (STAT3) phosphorylation, blocked STAT3 DNA binding, and down-regulated the expression of STAT3 downstream genes. Bazedoxifene also induced cell apoptosis, reduced cell viability, and inhibited colony formation in rhabdomyosarcoma cells. The inhibition of colony formation, STAT3 phosphorylation, or cell viability following Bazedoxifene treatment was partially reversed by addition of excess IL-6 or overexpression of constitutive STAT3, respectively, supporting Bazedoxifene acted through IL-6/GP130 signaling. In addition, Bazedoxifene repressed cell invasion and angiogenesis in vitro. Furthermore, oral administration of Bazedoxifene significantly suppressed tumor growth and expression of STAT3 phosphorylation in nude mice bearing established human rhabdomyosarcoma xenograft. Taken together, these findings validate IL-6/GP130 signaling as therapeutic target in rhabdomyosarcoma and provide first evidence that Bazedoxifene may serve as a novel promising drug targeting IL-6/GP130 for treatment of rhabdomyosarcoma.
[Mh] Termos MeSH primário: Receptor gp130 de Citocina/metabolismo
Indóis/farmacologia
Interleucina-6/metabolismo
Rabdomiossarcoma/tratamento farmacológico
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Ensaios de Seleção de Medicamentos Antitumorais
Células Endoteliais da Veia Umbilical Humana
Seres Humanos
Camundongos
Camundongos Nus
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Rabdomiossarcoma/metabolismo
Rabdomiossarcoma/patologia
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Indoles); 0 (Interleukin-6); 133483-10-0 (Cytokine Receptor gp130); Q16TT9C5BK (bazedoxifene)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170704
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180297


  6 / 1424 MEDLINE  
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[PMID]:28645526
[Au] Autor:Niemi JP; Filous AR; DeFrancesco A; Lindborg JA; Malhotra NA; Wilson GN; Zhou B; Crish SD; Zigmond RE
[Ad] Endereço:Department of Neurosciences, Case Western Reserve University, Cleveland, OH, USA.
[Ti] Título:Injury-induced gp130 cytokine signaling in peripheral ganglia is reduced in diabetes mellitus.
[So] Source:Exp Neurol;296:1-15, 2017 Oct.
[Is] ISSN:1090-2430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neuropathy is a major diabetic complication. While the mechanism of this neuropathy is not well understood, it is believed to result in part from deficient nerve regeneration. Work from our laboratory established that gp130 family of cytokines are induced in animals after axonal injury and are involved in the induction of regeneration-associated genes (RAGs) and in the conditioning lesion response. Here, we examine whether a reduction of cytokine signaling occurs in diabetes. Streptozotocin (STZ) was used to destroy pancreatic ß cells, leading to chronic hyperglycemia. Mice were injected with either low doses of STZ (5×60mg/kg) or a single high dose (1×200mg/kg) and examined after three or one month, respectively. Both low and high dose STZ treatment resulted in sustained hyperglycemia and functional deficits associated with the presence of both sensory and autonomic neuropathy. Diabetic mice displayed significantly reduced intraepidermal nerve fiber density and sudomotor function. Furthermore, low and high dose diabetic mice showed significantly reduced tactile touch sensation measured with Von Frey monofilaments. To look at the regenerative and injury-induced responses in diabetic mice, neurons in both superior cervical ganglia (SCG) and the 4th and 5th lumbar dorsal root ganglia (DRG) were unilaterally axotomized. Both high and low dose diabetic mice displayed significantly less axonal regeneration in the sciatic nerve, when measured in vivo, 48h after crush injury. Significantly reduced induction of two gp130 cytokines, leukemia inhibitory factor and interleukin-6, occurred in diabetic animals in SCG 6h after injury compared to controls. Injury-induced expression of interleukin-6 was also found to be significantly reduced in the DRG at 6h after injury in low and high dose diabetic mice. These effects were accompanied by reduced phosphorylation of signal transducer and activator of transcription 3 (STAT3), a downstream effector of the gp130 signaling pathway. We also found decreased induction of several gp130-dependent RAGs, including galanin and vasoactive intestinal peptide. Together, these data suggest a novel mechanism for the decreased response of diabetic sympathetic and sensory neurons to injury.
[Mh] Termos MeSH primário: Receptor gp130 de Citocina/metabolismo
Diabetes Mellitus Experimental/patologia
Regulação da Expressão Gênica/fisiologia
Degeneração Neural/etiologia
Transdução de Sinais/fisiologia
Gânglio Cervical Superior/metabolismo
[Mh] Termos MeSH secundário: Animais
Antibióticos Antineoplásicos/toxicidade
Glicemia/efeitos dos fármacos
Peso Corporal/efeitos dos fármacos
Receptor gp130 de Citocina/genética
Citocinas/metabolismo
Diabetes Mellitus Experimental/induzido quimicamente
Diabetes Mellitus Experimental/complicações
Modelos Animais de Doenças
Jejum/sangue
Hiperalgesia/etiologia
Hiperglicemia/etiologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Degeneração Neural/patologia
Proteínas do Tecido Nervoso/metabolismo
Medição da Dor
Transdução de Sinais/efeitos dos fármacos
Estreptozocina/toxicidade
Gânglio Cervical Superior/efeitos dos fármacos
Sudorese/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibiotics, Antineoplastic); 0 (Blood Glucose); 0 (Cytokines); 0 (Il6st protein, mouse); 0 (Nerve Tissue Proteins); 133483-10-0 (Cytokine Receptor gp130); 5W494URQ81 (Streptozocin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170822
[Lr] Data última revisão:
170822
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170625
[St] Status:MEDLINE


  7 / 1424 MEDLINE  
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[PMID]:28632778
[Au] Autor:Kammoun HL; Allen TL; Henstridge DC; Kraakman MJ; Peijs L; Rose-John S; Febbraio MA
[Ad] Endereço:Cellular and Molecular Metabolism Laboratory, Baker Heart & Diabetes Institute, Melbourne, Australia.
[Ti] Título:Over-expressing the soluble gp130-Fc does not ameliorate methionine and choline deficient diet-induced non alcoholic steatohepatitis in mice.
[So] Source:PLoS One;12(6):e0179099, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Non-alcoholic steatohepatitis (NASH) is a liver disease with the potential to lead to cirrhosis and hepatocellular carcinoma. Interleukin-6 (IL-6) has been implicated in the pathogenesis of NASH, with the so-called IL-6 'trans-signaling' cascade being responsible for the pro-inflammatory actions of this cytokine. We aimed to block IL-6 'trans-signaling', using a transgenic mouse that overexpresses human soluble glycoprotein130 (sgp130Fc Tg mice) fed a commonly used dietary model of inducing NASH (methionine and choline deficient-diet; MCD diet) and hypothesized that markers of NASH would be ameliorated in such mice. Sgp130Fc Tg and littermate control mice were fed a MCD or control diet for 4 weeks. The MCD diet induced many hallmarks of NASH including hepatomegaly, steatosis, and liver inflammation. However, in contrast with other mouse models and, indeed, human NASH, the MCD diet model did not increase the mRNA or protein expression of IL-6. Not surprisingly, therefore, markers of MCD diet-induced NASH were unaffected by sgp130Fc transgenic expression. While the MCD diet model induces many pathophysiological markers of NASH, it does not induce increased IL-6 expression in the liver, a key hallmark of human NASH. We, therefore, caution the use of the MCD diet as a viable mouse model of NASH.
[Mh] Termos MeSH primário: Deficiência de Colina
Receptor gp130 de Citocina/administração & dosagem
Modelos Animais de Doenças
Inflamação/patologia
Interleucina-6/metabolismo
Metionina/deficiência
Hepatopatia Gordurosa não Alcoólica/patologia
[Mh] Termos MeSH secundário: Animais
Biomarcadores/metabolismo
Suplementos Nutricionais
Seres Humanos
Inflamação/induzido quimicamente
Inflamação/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Hepatopatia Gordurosa não Alcoólica/induzido quimicamente
Hepatopatia Gordurosa não Alcoólica/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Interleukin-6); 133483-10-0 (Cytokine Receptor gp130); AE28F7PNPL (Methionine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170621
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0179099


  8 / 1424 MEDLINE  
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[PMID]:28557957
[Au] Autor:Zhang H; Huang E; Kahwaji J; Nast CC; Li P; Mirocha J; Thomas DL; Ge S; Vo AA; Jordan SC; Toyoda M
[Ad] Endereço:1 Transplant Immunology Laboratory, Cedars-Sinai Medical Center, Los Angeles, CA. 2 Comprehensive Transplant Center, Cedars-Sinai Medical Center, Los Angeles, CA. 3 Department of Nephrology, Kaiser-Permanente Los Angeles Medical Center, Los Angeles, CA. 4 Department of Pathology and Laboratory Medicine, Cedars-Sinai Medical Center, Los Angeles, CA. 5 Department of Surgery, Cedars-Sinai Medical Center, Los Angeles, CA. 6 Biostatistics and Bioinformatics Research Center, Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, CA.
[Ti] Título:Plasma Exosomes From HLA-Sensitized Kidney Transplant Recipients Contain mRNA Transcripts Which Predict Development of Antibody-Mediated Rejection.
[So] Source:Transplantation;101(10):2419-2428, 2017 Oct.
[Is] ISSN:1534-6080
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Sensitization to HLA remains a significant immunologic barrier to successful transplantation. Identifying immune mechanisms responsible for antibody-mediated rejection (AMR) is an important goal. Here, we explored the possibility of predicting the risk for AMR by measuring mRNA transcripts of AMR-associated genes in plasma exosomes from kidney transplant patients. METHODS: Total RNA was extracted from exosomes purified from 152 ethylenediaminetetraacetic acid-plasma samples of 64 patients (18 AMR, 8 cell-mediated rejection [CMR], 38 no rejection in desensitized [DES] and non-DES control groups) for reverse transcription into cDNA, preamplification and then real time quantitative polymerase chain reaction (qPCR) for 21 candidate genes. The mRNA transcript levels of each gene were calculated. Comparisons were made among 4 patient groups for each gene and also for a gene combination score based on selected genes. RESULTS: Among 21 candidate genes, we identified multiple genes (gp130, CCL4, TNFα, SH2D1B, CAV1, atypical chemokine receptor 1 [duffy blood group]) whose mRNA transcript levels in plasma exosomes significantly increased among AMR compared with CMR and/or control patients. A gene combination score calculated from 4 genes of gp130, SH2D1B, TNFα, and CCL4 was significantly higher in the AMR than the CMR (P < 0.0001) and no rejection control groups (P < 0.01 vs DES control, P < 0.05 vs non-DES control). CONCLUSIONS: Our results suggest that plasma exosomes may contain information indicating clinical conditions of kidney transplant patients. mRNA transcript profiles based on gp130, SH2D1B, TNFα, and CCL4 in plasma exosomes may be used to predict on-going and/or imminent AMR.
[Mh] Termos MeSH primário: Exossomos/metabolismo
Rejeição de Enxerto/sangue
Antígenos HLA/imunologia
Histocompatibilidade
Isoanticorpos/sangue
Transplante de Rim/efeitos adversos
RNA Mensageiro/sangue
[Mh] Termos MeSH secundário: Adulto
Estudos de Casos e Controles
Quimiocina CCL4/genética
Receptor gp130 de Citocina/genética
Exossomos/genética
Feminino
Perfilação da Expressão Gênica/métodos
Marcadores Genéticos
Rejeição de Enxerto/genética
Rejeição de Enxerto/imunologia
Seres Humanos
Masculino
Meia-Idade
Valor Preditivo dos Testes
RNA Mensageiro/genética
Reação em Cadeia da Polimerase em Tempo Real
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Medição de Risco
Fatores de Risco
Fatores de Transcrição/genética
Resultado do Tratamento
Fator de Necrose Tumoral alfa/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCL4 protein, human); 0 (Chemokine CCL4); 0 (Genetic Markers); 0 (HLA Antigens); 0 (IL6ST protein, human); 0 (Isoantibodies); 0 (RNA, Messenger); 0 (SH2D1B protein, human); 0 (Transcription Factors); 0 (Tumor Necrosis Factor-alpha); 133483-10-0 (Cytokine Receptor gp130)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170531
[St] Status:MEDLINE
[do] DOI:10.1097/TP.0000000000001834


  9 / 1424 MEDLINE  
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[PMID]:28402851
[Au] Autor:Timper K; Denson JL; Steculorum SM; Heilinger C; Engström-Ruud L; Wunderlich CM; Rose-John S; Wunderlich FT; Brüning JC
[Ad] Endereço:Max Planck Institute for Metabolism Research, Department of Neuronal Control of Metabolism, Gleueler Str. 50, 50931 Cologne, Germany; Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), University Hospital Cologne, Kerpener Str. 26, 50924 Cologne, Germany; Excellence Cluster on Cellul
[Ti] Título:IL-6 Improves Energy and Glucose Homeostasis in Obesity via Enhanced Central IL-6 trans-Signaling.
[So] Source:Cell Rep;19(2):267-280, 2017 Apr 11.
[Is] ISSN:2211-1247
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Interleukin (IL)-6 engages similar signaling mechanisms to leptin. Here, we find that central application of IL-6 in mice suppresses feeding and improves glucose tolerance. In contrast to leptin, whose action is attenuated in obesity, the ability of IL-6 to suppress feeding is enhanced in obese mice. IL-6 suppresses feeding in the absence of neuronal IL-6-receptor (IL-6R) expression in hypothalamic or all forebrain neurons of mice. Conversely, obese mice exhibit increased soluble IL-6R levels in the cerebrospinal fluid. Blocking IL-6 trans-signaling in the CNS abrogates the ability of IL-6 to suppress feeding. Furthermore, gp130 expression is enhanced in the paraventricular nucleus of the hypothalamus (PVH) of obese mice, and deletion of gp130 in the PVH attenuates the beneficial central IL-6 effects on metabolism. Collectively, these experiments indicate that IL-6 trans-signaling is enhanced in the CNS of obese mice, allowing IL-6 to exert its beneficial metabolic effects even under conditions of leptin resistance.
[Mh] Termos MeSH primário: Fenômenos Fisiológicos da Nutrição Animal/genética
Receptor gp130 de Citocina/genética
Interleucina-6/genética
Obesidade/genética
[Mh] Termos MeSH secundário: Animais
Receptor gp130 de Citocina/biossíntese
Metabolismo Energético/genética
Glucose/metabolismo
Seres Humanos
Hipotálamo/metabolismo
Hipotálamo/patologia
Interleucina-6/metabolismo
Camundongos
Camundongos Obesos
Neurônios/metabolismo
Neurônios/patologia
Obesidade/metabolismo
Obesidade/fisiopatologia
Prosencéfalo/metabolismo
Prosencéfalo/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-6); 0 (interleukin-6, mouse); 133483-10-0 (Cytokine Receptor gp130); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170501
[Lr] Data última revisão:
170501
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170414
[St] Status:MEDLINE


  10 / 1424 MEDLINE  
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[PMID]:28315013
[Au] Autor:Al-Quraishy S; Dkhil MA; Abdel-Baki AS; Ghanjati F; Erichsen L; Santourlidis S; Wunderlich F; Araúzo-Bravo MJ
[Ad] Endereço:Department of Zoology, College of Science, King Saud University, P.O. Box 2455, Riyadh, 11451, Saudi Arabia. guraishi@yahoo.com.
[Ti] Título:Protective vaccination and blood-stage malaria modify DNA methylation of gene promoters in the liver of Balb/c mice.
[So] Source:Parasitol Res;116(5):1463-1477, 2017 May.
[Is] ISSN:1432-1955
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Epigenetic mechanisms such as DNA methylation are increasingly recognized to be critical for vaccination efficacy and outcome of different infectious diseases, but corresponding information is scarcely available for host defense against malaria. In the experimental blood-stage malaria Plasmodium chabaudi, we investigate the possible effects of a blood-stage vaccine on DNA methylation of gene promoters in the liver, known as effector against blood-stage malaria, using DNA methylation microarrays. Naturally susceptible Balb/c mice acquire, by protective vaccination, the potency to survive P. chabaudi malaria and, concomitantly, modifications of constitutive DNA methylation of promoters of numerous genes in the liver; specifically, promoters of 256 genes are hyper(=up)- and 345 genes are hypo(=down)-methylated (p < 0.05). Protective vaccination also leads to changes in promoter DNA methylation upon challenge with P. chabaudi at peak parasitemia on day 8 post infection (p.i.), when 571 and 1013 gene promoters are up- and down-methylated, respectively, in relation to constitutive DNA methylation (p < 0.05). Gene set enrichment analyses reveal that both vaccination and P. chabaudi infections mainly modify promoters of those genes which are most statistically enriched with functions relating to regulation of transcription. Genes with down-methylated promoters encompass those encoding CX3CL1, GP130, and GATA2, known to be involved in monocyte recruitment, IL-6 trans-signaling, and onset of erythropoiesis, respectively. Our data suggest that vaccination may epigenetically improve parts of several effector functions of the liver against blood-stage malaria, as, e.g., recruitment of monocyte/macrophage to the liver accelerated liver regeneration and extramedullary hepatic erythropoiesis, thus leading to self-healing of otherwise lethal P. chabaudi blood-stage malaria.
[Mh] Termos MeSH primário: Metilação de DNA/genética
Fígado/metabolismo
Macrófagos/imunologia
Vacinas Antimaláricas/imunologia
Malária/imunologia
Monócitos/imunologia
Plasmodium chabaudi/imunologia
[Mh] Termos MeSH secundário: Animais
Quimiocina CX3CL1/biossíntese
Quimiocina CX3CL1/genética
Receptor gp130 de Citocina/biossíntese
Receptor gp130 de Citocina/genética
Epigênese Genética
Feminino
Fator de Transcrição GATA2/biossíntese
Fator de Transcrição GATA2/genética
Interleucina-6/genética
Malária/parasitologia
Malária/prevenção & controle
Camundongos
Camundongos Endogâmicos BALB C
Análise de Sequência com Séries de Oligonucleotídeos
Parasitemia/imunologia
Regiões Promotoras Genéticas/genética
Vacinação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokine CX3CL1); 0 (Cx3cl1 protein, mouse); 0 (GATA2 Transcription Factor); 0 (Gata2 protein, mouse); 0 (Il6st protein, mouse); 0 (Interleukin-6); 0 (Malaria Vaccines); 133483-10-0 (Cytokine Receptor gp130)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171007
[Lr] Data última revisão:
171007
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170319
[St] Status:MEDLINE
[do] DOI:10.1007/s00436-017-5423-0



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