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[PMID]:28448456
[Au] Autor:Othumpangat S; Bryan NB; Beezhold DH; Noti JD
[Ad] Endereço:Allergy and Clinical Immunology Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Centers for Disease Control and Prevention, Morgantown, WV 26505, USA. seo8@cdc.gov.
[Ti] Título:Upregulation of miRNA-4776 in Influenza Virus Infected Bronchial Epithelial Cells Is Associated with Downregulation of NFKBIB and Increased Viral Survival.
[So] Source:Viruses;9(5), 2017 04 27.
[Is] ISSN:1999-4915
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Influenza A virus (IAV) infection remains a significant cause of morbidity and mortality worldwide. One key transcription factor that is activated upon IAV infection is nuclear factor Kappa B (NF-κB). NF-κB regulation involves the inhibitor proteins NF-κB inhibitor beta (NFKBIB), (also known as IκB ß), which form complexes with NF-κB to sequester it in the cytoplasm. In this study, microarray data showed differential expression of several microRNAs (miRNAs) on exposure to IAV. Target scan analysis revealed that miR-4776, miR-4514 and miR-4742 potentially target NFKBIB messenger RNA (mRNA). Time-course analysis of primary bronchial epithelial cells (HBEpCs) showed that miR-4776 expression is increased within 1 h of infection, followed by its downregulation 4 h post-exposure to IAV. NFKBIB upregulation of miR-4776 correlated with a decrease in NFKBIB expression within 1 h of infection and a subsequent increase in NFKBIB expression 4 h post-infection. In addition, miRNA ago-immunoprecipitation studies and the three prime untranslated region (3' UTR) luciferase assay confirmed that miR-4776 targets NFKBIB mRNA. Furthermore, uninfected HBEpCs transfected with miR-4776 mimic showed decreased expression of NFKBIB mRNA. Overexpression of NFKBIB protein in IAV infected cells led to lower levels of IAV. Taken together, our data suggest that miRNA-4776 modulates IAV production in infected cells through NFKBIB expression, possibly through the modulation of NF-κB.
[Mh] Termos MeSH primário: Brônquios/virologia
Células Epiteliais/virologia
Proteínas I-kappa B/genética
Vírus da Influenza A Subtipo H1N1/fisiologia
MicroRNAs/genética
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Brônquios/citologia
Linhagem Celular
Regulação para Baixo
Regulação da Expressão Gênica
Seres Humanos
Proteínas I-kappa B/metabolismo
Análise em Microsséries
Viabilidade Microbiana
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Transdução de Sinais
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (I kappa B beta protein); 0 (I-kappa B Proteins); 0 (MicroRNAs); 0 (RNA, Messenger)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE


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[PMID]:28873611
[Au] Autor:Zhang Y; Liu D; Fang L; Zhao X; Zhou A; Xie J
[Ad] Endereço:College of Biotechnology and Food Science, Tianjin University of Commerce, Tianjin Key Laboratory of Food Biotechnology, Tianjin 300134, China.
[Ti] Título:A galactomannoglucan derived from Agaricus brasiliensis: Purification, characterization and macrophage activation via MAPK and IκB/NFκB pathways.
[So] Source:Food Chem;239:603-611, 2018 Jan 15.
[Is] ISSN:0308-8146
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In this study, a novel galactomannoglucan named as TJ2 was isolated from Agaricus brasiliensis with microwave extraction, macroporous resin, ion exchange resin and high resolution gel chromatography. TJ2 is composed of glucose, mannose and galactose in the ratio 99.2:0.2:0.6. Infrared spectra (IR), methylation analysis and nuclear magnetic resonance spectra indicated that TJ2 mainly contained a ß-(1→3) - linked glucopyranosyl backbone. Interestingly, TJ2 significantly promoted RAW264.7 cell proliferation, and was able to activate the cells to engulf E. coli. In addition, TJ2 induced the expression of Interleukin 1ß (IL-1ß), Interleukin 6 (IL-6), tumor necrosis factor α (TNF-α) and cyclooxygenase-2 (Cox-2) in the cells. TJ2 also promoted the production of nitric oxide (NO) by inducing the expression of inducible nitric oxide synthase (iNOS). Moreover, TJ2 is a potent inducer in activating the mitogen-activated protein kinase (MAPK) and inhibitor of nuclear factor-kappa B (IκB)/nuclear factor-kappa B (NFκB) pathways.
[Mh] Termos MeSH primário: Agaricus
[Mh] Termos MeSH secundário: Ciclo-Oxigenase 2
Escherichia coli
Proteínas I-kappa B
Lipopolissacarídeos
Ativação de Macrófagos
NF-kappa B
Óxido Nítrico
Óxido Nítrico Sintase Tipo II
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (I-kappa B Proteins); 0 (Lipopolysaccharides); 0 (NF-kappa B); 31C4KY9ESH (Nitric Oxide); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 1.14.99.1 (Cyclooxygenase 2)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170907
[St] Status:MEDLINE


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[PMID]:28892747
[Au] Autor:Duan JX; Zhou Y; Zhou AY; Guan XX; Liu T; Yang HH; Xie H; Chen P
[Ad] Endereço:Department of Respiratory Medicine, The Second Xiangya Hospital, Central South University, Changsha 410011, Hunan, China; Research Unit of Respiratory Disease, Central South University, Changsha 410011, Hunan, China; Diagnosis and Treatment Center of Respiratory Disease, Central South University, Ch
[Ti] Título:Calcitonin gene-related peptide exerts anti-inflammatory property through regulating murine macrophages polarization in vitro.
[So] Source:Mol Immunol;91:105-113, 2017 11.
[Is] ISSN:1872-9142
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Acute lung injury (ALI) is a condition resulting from direct or indirect lung injury associated with high mortality and morbidity. The phenotype of macrophages in lung contributes to the pathological progress of ALI. Calcitonin gene-related peptide (CGRP) is one of the most abundant neuropeptides in lung, and attenuates lipopolysaccharide (LPS)-induced ALI in rats. However, the exact effect of CGRP on the activation of macrophages remains unknown. Here we investigate the effect of CGRP on the macrophages activation and inflammation in murine macrophages in vitro. We found that LPS increased the expression of CGRP in a LPS-induced ALI murine model and LPS-stimulated murine macrophages. Although CGRP didn't alter the expression of tumor necrosis factor-α (a marker of pro-inflammatory phenotype of macrophages, M1 macrophages) or Arginase 1 (Arg1, a marker of M2 macrophages) in non-differentiated macrophages, CGRP significantly reduced the NLRP3 and pro-IL-1ß mRNA expression induced by LPS, as well as NLRP3 protein and IL-1ß secretion induced by LPS+ATP in macrophages in vitro. On the other hand, CGRP dramatically enhanced the Arg1 expression and activity induced by IL-4 in the time- and dose-dependent manners. CGRP also promoted the expression of markers of M2 macrophages (IL-10, Fizz1 and Mrc1) induced by IL-4 in murine macrophages. These effects of CGRP were also observed in primary murine peritoneal macrophages. In addition, we found that CGRP regulated macrophages polarization partially through calmodulin, PKC and PKA pathways. Specifically, CGRP could inhibit the degradation of I-κB induced by LPS, and enhance the phosphorylation of STAT6 induced by IL-4 in macrophages. In conclusion, our results indicate that CGRP regulates macrophage polarization and inhibits inflammation in murine macrophages.
[Mh] Termos MeSH primário: Lesão Pulmonar Aguda/imunologia
Peptídeo Relacionado com Gene de Calcitonina/imunologia
Macrófagos/imunologia
[Mh] Termos MeSH secundário: Lesão Pulmonar Aguda/induzido quimicamente
Lesão Pulmonar Aguda/patologia
Animais
Antígenos de Diferenciação/imunologia
Citocinas/imunologia
Modelos Animais de Doenças
Proteínas I-kappa B/imunologia
Lipopolissacarídeos/toxicidade
Macrófagos/patologia
Masculino
Camundongos
Ratos
Fator de Transcrição STAT6/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, Differentiation); 0 (Cytokines); 0 (I-kappa B Proteins); 0 (Lipopolysaccharides); 0 (STAT6 Transcription Factor); 0 (Stat6 protein, mouse); 83652-28-2 (Calcitonin Gene-Related Peptide)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171120
[Lr] Data última revisão:
171120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170912
[St] Status:MEDLINE


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[PMID]:28694207
[Au] Autor:Liao Z; Wang J; Tan H; Wei L
[Ad] Endereço:Affiliated Hospital of YouJiang Medical University for Nationalities, Baise, Guangxi 533000, PR China; The Second Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530007, PR China.
[Ti] Título:Cinnamon extracts exert intrapancreatic cytoprotection against streptozotocin in vivo.
[So] Source:Gene;627:519-523, 2017 Sep 05.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:In the current study, we aimed to investigate the potential hypoglycemic bioactivity of cinnamon extracts (CES) on streptozotocin (STZ)-induced hyperglycemia in mice. In biological methods, glucose metabolic ability of all mice was evaluated by glucose tolerance testing (GTT). Blood levels of pancreas-produced insulin, glucagon, inflammation-associated interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) were determined via enzyme-linked immunosorbent assay (ELISA). In gene level, intrapancreatic mRNA expressions of insulin, TNF-α and nuclear-factor kappa B (NF-κB) were assayed by reverse transcription polymerase chain reaction (RT-PCR). Meanwhile, intracellular insulin-immunoactive cells in the pancreas were analyzed by using immunohistochemical staining. In addition, the protein levels of intrapancreatic NF-κB, IκB (p-IκB) and IKK were tested by western blotting. As a result, CES-treated mice showed increased body weight, blood glucose and insulin, reduced IL-6 and TNF-α contents in sera. Further, the TNF-α and NF-κB mRNA expressions in the CES-treated pancreas were down-regulated at a dose-dependent manner, while insulin mRNA was elevated. Moreover, the reduced intrapancreatic NF-κB, IκB (p-IκB) and IKK expression were observed in CES-treated pancreas, respectively. Taken together, our current findings indicate that CES-mediated intrapancreatic cytoprotection is linked to the molecular mechanism that may be through inhibiting inflammatory stress and promoting insulin secretion in the pancreas.
[Mh] Termos MeSH primário: Cinnamomum zeylanicum/química
Hiperglicemia/tratamento farmacológico
Pâncreas/efeitos dos fármacos
Extratos Vegetais/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Hiperglicemia/etiologia
Hiperglicemia/metabolismo
Quinase I-kappa B/genética
Quinase I-kappa B/metabolismo
Proteínas I-kappa B/genética
Proteínas I-kappa B/metabolismo
Insulina/secreção
Interleucina-6/genética
Interleucina-6/metabolismo
Camundongos
NF-kappa B/genética
NF-kappa B/metabolismo
Pâncreas/metabolismo
Extratos Vegetais/farmacologia
Estreptozocina/toxicidade
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (I kappa B beta protein); 0 (I-kappa B Proteins); 0 (Insulin); 0 (Interleukin-6); 0 (NF-kappa B); 0 (Plant Extracts); 0 (Tumor Necrosis Factor-alpha); 5W494URQ81 (Streptozocin); EC 2.7.11.10 (I-kappa B Kinase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170712
[St] Status:MEDLINE


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[PMID]:28670959
[Au] Autor:Li D; Wu C; Cai Y; Liu B
[Ad] Endereço:1 Fujian Health College, Fuzhou, China.
[Ti] Título:Association of NFKB1 and NFKBIA gene polymorphisms with susceptibility of gastric cancer.
[So] Source:Tumour Biol;39(7):1010428317717107, 2017 Jul.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Xianyou county of Fujian province, located on the southeast coastal of China, has higher gastric cancer mortality. Chronic inflammation plays an important role in the occurrence of gastric cancer, in which the nuclear factor-κB signaling pathway of the inflammatory reaction begins and plays an important role in the amplification process. Studies have found that a single-nucleotide polymorphism of nuclear factor-κB signaling pathway molecules encoding genes is associated with gastric cancer, but the combined effect of the nuclear factor-κB signaling pathway gene has not been explained nor has been cardia and non-cardia gastric cancer risk factors and genetic susceptibility loci. New gastric cancer cases of the Fujian Xianyou Hospital were the research object. They were divided into cardia and non-cardia cancer in order to study a single-nucleotide polymorphism of the nuclear factor-κB signaling pathway important node molecules P50 and I kappa B encoding genes NFKB1 and NFKBIA by desorption ionization time of flight mass spectrometry analysis and by matrix-assisted laser mass spectrometry. The results showed that NFKB1 and NFKBIA single-nucleotide polymorphisms and gastric cancer are related and that the combined effects of polymorphisms in two genes and the NFKBIA gene monomer increased the risk of gastric cancer, and it was found that in different types of gastric cancer (the cardia and non-cardia cancer), susceptible polymorphism sites and combined effects are different.
[Mh] Termos MeSH primário: Estudos de Associação Genética
Proteínas I-kappa B/genética
Subunidade p50 de NF-kappa B/genética
Neoplasias Gástricas/genética
[Mh] Termos MeSH secundário: China
Feminino
Predisposição Genética para Doença
Genótipo
Haplótipos/genética
Seres Humanos
Masculino
Inibidor de NF-kappaB alfa
NF-kappa B/genética
Polimorfismo de Nucleotídeo Único
Fatores de Risco
Neoplasias Gástricas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (I-kappa B Proteins); 0 (NF-kappa B); 0 (NF-kappa B p50 Subunit); 0 (NFKB1 protein, human); 0 (NFKBIA protein, human); 139874-52-5 (NF-KappaB Inhibitor alpha)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170704
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317717107


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[PMID]:28545815
[Au] Autor:Janganati V; Ponder J; Thakkar S; Jordan CT; Crooks PA
[Ad] Endereço:Department of Pharmaceutical Sciences, College of Pharmacy, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.
[Ti] Título:Succinamide derivatives of melampomagnolide B and their anti-cancer activities.
[So] Source:Bioorg Med Chem;25(14):3694-3705, 2017 Jul 15.
[Is] ISSN:1464-3391
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A series of succinamide derivatives of melampomagnolide B have been synthesized by coupling MMB monosuccinate (2) with various heterocyclic amines to afford compounds 3a-3l. MMB monosuccinate was also reacted with terminal diaminoalkanes to afford dimeric succinamido analogs of MMB (4a-4h). These succinamide analogs of MMB were evaluated for their anti-cancer activity against a panel of sixty human cancer cell lines. Analogs 3d-3i and dimers 4f-4g exhibited promising anti-cancer activity with GI values ranging from 0.28 to 33.5µM against most of the cell lines in the panel. The dimeric analogs 4f and 4g were identified as lead compounds with GI values in the nanomolar range (GI =280-980nM) against several cell lines in the panel; i.e. leukemia cell lines CCRF-CEM, HL-60(TB), K-562, MOLT-4, RPMI-8226 and SR; and solid tumor cell lines NCI-H522 (non-small cell lung cancer), SW-620 and HCT-116 (colon cancer), LOX IMVI (melanoma), RXF 393 (renal cancer), and MCF7, BT-549 and MDA-MB-468 (breast cancer). Succinamide analogs 3a, 3c-3l and 4b-4h were also evaluated for their apoptotic activity against M9-ENL1 acute myelogenous leukemia cells; compounds 3h-3j and 4g were equipotent with parthenolide, exhibiting LC values in the range 4.1-8.1µM. Molecular docking studies indicate that these molecules interact covalently with the highly conserved Cys-46 residue of the N-terminal lobe (1-109) of human IKKß to inhibit the NFκB transcription factor complex, resulting in down-regulation of anti-apoptotic genes under NFκB control.
[Mh] Termos MeSH primário: Amidas/química
Sesquiterpenos/química
Succinatos/química
[Mh] Termos MeSH secundário: Antineoplásicos/síntese química
Antineoplásicos/química
Antineoplásicos/farmacologia
Apoptose/efeitos dos fármacos
Sítios de Ligação
Linhagem Celular Tumoral
Regulação para Baixo/efeitos dos fármacos
Ensaios de Seleção de Medicamentos Antitumorais
Seres Humanos
Proteínas I-kappa B/antagonistas & inibidores
Proteínas I-kappa B/metabolismo
Simulação de Acoplamento Molecular
Estrutura Terciária de Proteína
Sesquiterpenos/síntese química
Sesquiterpenos/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amides); 0 (Antineoplastic Agents); 0 (I kappa B beta protein); 0 (I-kappa B Proteins); 0 (Sesquiterpenes); 0 (Succinates); 0 (melampomagnolide B); Y656F4N881 (succinamide)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170527
[St] Status:MEDLINE


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[PMID]:28526689
[Au] Autor:Fang L; Sun J; Pan Z; Song Y; Zhong L; Zhang Y; Liu Y; Zheng X; Huang P
[Ad] Endereço:Department of Pharmacy, Zhejiang Cancer Hospital, Hangzhou, China.
[Ti] Título:Long non-coding RNA NEAT1 promotes hepatocellular carcinoma cell proliferation through the regulation of miR-129-5p-VCP-IκB.
[So] Source:Am J Physiol Gastrointest Liver Physiol;313(2):G150-G156, 2017 Aug 01.
[Is] ISSN:1522-1547
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Long non-coding RNA nuclear-enriched abundant transcript 1 (NEAT1) plays an important role in the pathogenesis and development of several types of cancer. However, the functional mechanism of NEAT1 in hepatocellular carcinoma (HCC) remains unclear. NEAT1 and microRNA (miR)-129-5p expression in HCC tissues and cell lines was quantified by means of quantitative PCR. The effects of NEAT1 expression inhibition or upregulation in HCC cell lines were analyzed in terms of cell viability and apoptosis. Biological software was used to predict the binding sites of NEAT1 and miR-129-5p. The expression of the miR-129-5p target molecules valosin-containing protein (VCP) and IκB was detected using Western blotting. The effect of NEAT1 on tumor growth was observed in mouse models of transplanted hepatoma. In the present study, it was concluded that the expression of NEAT1 was significantly increased in the HCC tissues and cell lines. Meanwhile, after downregulating NEAT1 expression in HepG2/Huh7 cell lines, the cell viability was significantly lowered, whereas the corresponding rate of apoptosis was significantly increased. Additionally, it was found that the NEAT1 and miR-129-5p expression showed a negative correlation in HCC tissues. It was further proved that there was a certain negative regulatory mechanism between NEAT1 and miR-129-5p, which was related to the expression of VCP and IκB. The mouse model experiments confirmed that the interference with NEAT1 expression inhibited tumor growth. The study concluded that the overexpression of NEAT1 inhibited the expression of miR-129-5p by regulating VCP/IκB, thereby promoting the proliferation of HCC cells. This study provides new insights into the pathogenesis of HCC, as well as identifying new target genes for diagnosis and treatment. The results provide strong evidence that upregulated NEAT1 promotes the proliferation of cancer cells in hepatocellular carcinoma (HCC) and this regulatory mechanism depends on the microRNA (miR)-129-5p-valosin-containing protein-IκB axis. The study also indicates that NEAT1 could be a potential therapeutic target for HCC.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/genética
Proliferação Celular/genética
Regulação Neoplásica da Expressão Gênica
Neoplasias Hepáticas/genética
MicroRNAs/genética
RNA Longo não Codificante/genética
[Mh] Termos MeSH secundário: Adenosina Trifosfatases/genética
Adenosina Trifosfatases/metabolismo
Animais
Carcinoma Hepatocelular/metabolismo
Carcinoma Hepatocelular/patologia
Proteínas de Ciclo Celular/genética
Proteínas de Ciclo Celular/metabolismo
Células Hep G2
Seres Humanos
Proteínas I-kappa B/genética
Proteínas I-kappa B/metabolismo
Neoplasias Hepáticas/metabolismo
Neoplasias Hepáticas/patologia
Camundongos
Camundongos Nus
MicroRNAs/metabolismo
RNA Longo não Codificante/metabolismo
Transdução de Sinais/genética
Proteína com Valosina
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cell Cycle Proteins); 0 (I-kappa B Proteins); 0 (MicroRNAs); 0 (Mirn129 microRNA, human); 0 (NEAT1 long non-coding RNA, human); 0 (RNA, Long Noncoding); EC 3.6.1.- (Adenosine Triphosphatases); EC 3.6.4.6 (VCP protein, human); EC 3.6.4.6 (Valosin Containing Protein); EC 3.6.4.6 (Vcp protein, mouse)
[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:170521
[St] Status:MEDLINE
[do] DOI:10.1152/ajpgi.00426.2016


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[PMID]:28476620
[Au] Autor:Wen Y; Yu Y; Fu X
[Ad] Endereço:Department of Neurosurgery, The First People's Hospital of ZunYi, ZunYi, China.
[Ti] Título:LncRNA Gm4419 contributes to OGD/R injury of cerebral microglial cells via IκB phosphorylation and NF-κB activation.
[So] Source:Biochem Biophys Res Commun;487(4):923-929, 2017 Jun 10.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ischemic stroke is one of major causes of adult morbidity. Recent studies have shown that over-activated microglial cells play a critical role in aggravating cerebral oxygen glucose deprivation/reoxygenation (OGD/R) damage by releasing excessive inflammatory cytokines. However, the involving mechanisms are not distinct yet. Long non-coding RNAs (lncRNAs) have been reported to in participate in lots of complicated biological processes. Our understandings of the relationship between lncRNAs and OGD/R injury are largely limited. In this study, we demonstrated that a lncRNA Gm4419 functioned as a crucial mediator in the activation of NF-κB signaling pathway, causing neuroinflammation damage during OGD/R. Gm4419 was abnormally up-regulated in OGD/R-treated microglial cells. We found that the high level of Gm4419 promoted the phosphorylation of IκBα by physically associating with IκBα, therefore, led to increased nucleus NF-κB levels for the transcriptional activation of TNF-α, IL-1ß and IL-6. In addition, we also demonstrated that knockdown of Gm4419 functioned as NF-κB inhibitor in OGD/R microglial cells, showing that down-regulation of Gm4419 had protective role against OGD/R injury. In summary, Gm4419 is required for microglial cell OGD/R injury though the activation of NF-κB signaling. Thus, Gm4419 appears to be a promising therapeutic target for ischemic stroke.
[Mh] Termos MeSH primário: Isquemia Encefálica/metabolismo
Isquemia Encefálica/patologia
Glucose/metabolismo
Proteínas I-kappa B/metabolismo
Microglia/metabolismo
NF-kappa B/metabolismo
RNA Longo não Codificante/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Camundongos
Microglia/patologia
Oxigênio/metabolismo
Fosforilação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (I-kappa B Proteins); 0 (NF-kappa B); 0 (RNA, Long Noncoding); IY9XDZ35W2 (Glucose); S88TT14065 (Oxygen)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170507
[St] Status:MEDLINE


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[PMID]:28438776
[Au] Autor:Lundh M; Bugliani M; Dahlby T; Chou DH; Wagner B; Ghiasi SM; De Tata V; Chen Z; Lund MN; Davies MJ; Marchetti P; Mandrup-Poulsen T
[Ad] Endereço:Department of Biomedical SciencesUniversity of Copenhagen, Copenhagen, Denmark.
[Ti] Título:The immunoproteasome is induced by cytokines and regulates apoptosis in human islets.
[So] Source:J Endocrinol;233(3):369-379, 2017 Jun.
[Is] ISSN:1479-6805
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In addition to degrading misfolded and damaged proteins, the proteasome regulates the fate of cells in response to stress. The role of the proteasome in pro-inflammatory cytokine-induced human beta-cell apoptosis is unknown. Using INS-1, INS-1E and human islets exposed to combinations of IFNγ, IL-1ß and TNFα with or without addition of small molecules, we assessed the role of the immunoproteasome in pancreatic beta-cell demise. Here, we show that cytokines induce the expression and activity of the immuno-proteasome in INS-1E cells and human islets. Cytokine-induced expression of immuno-proteasome subunits, but not activity, depended upon histone deacetylase 3 activation. Inhibition of JAK1/STAT1 signaling did not affect proteasomal activity. Inhibition of the immuno-proteasome subunit PSMB8 aggravated cytokine-induced human beta-cell apoptosis while reducing intracellular levels of oxidized proteins in INS-1 cells. While cytokines increased total cellular NFκB subunit P50 and P52 levels and reduced the cytosolic NFκB subunit P65 and IκB levels, these effects were unaffected by PSMB8 inhibition. We conclude that beta cells upregulate immuno-proteasome expression and activity in response to IFNγ, likely as a protective response to confine inflammatory signaling.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Citocinas/fisiologia
Ilhotas Pancreáticas/enzimologia
Complexo de Endopeptidases do Proteassoma/metabolismo
[Mh] Termos MeSH secundário: Histona Desacetilases/fisiologia
Seres Humanos
Proteínas I-kappa B/metabolismo
Janus Quinase 1/metabolismo
NF-kappa B/metabolismo
Fator de Transcrição STAT1/metabolismo
Transdução de Sinais/efeitos dos fármacos
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (I-kappa B Proteins); 0 (NF-kappa B); 0 (STAT1 Transcription Factor); 0 (STAT1 protein, human); EC 2.7.10.2 (JAK1 protein, human); EC 2.7.10.2 (Janus Kinase 1); EC 3.4.25.1 (LMP7 protein); EC 3.4.25.1 (Proteasome Endopeptidase Complex); EC 3.5.1.98 (Histone Deacetylases); EC 3.5.1.98 (histone deacetylase 3)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170717
[Lr] Data última revisão:
170717
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170426
[St] Status:MEDLINE
[do] DOI:10.1530/JOE-17-0110


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[PMID]:28436225
[Au] Autor:Zhuang L; Chen LF; Zhang YB; Liu Z; Xiao XH; Tang W; Wang GC; Song WJ; Li YL; Li MM
[Ad] Endereço:Institute of Traditional Chinese Medicine and Natural Products, College of Pharmacy, and ‡Guangdong Provincial Key Laboratory of Bioengineering Medicine, College of Life Science and Technology, Jinan University , Guangzhou, Guangdong 510632, People's Republic of China.
[Ti] Título:Watsonianone A from Rhodomyrtus tomentosa Fruit Attenuates Respiratory-Syncytial-Virus-Induced Inflammation In Vitro.
[So] Source:J Agric Food Chem;65(17):3481-3489, 2017 May 03.
[Is] ISSN:1520-5118
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Respiratory syncytial virus (RSV) is one of the most common respiratory pathogens. Immoderate inflammation plays a great role in causing RSV-induced diseases. In the present study, watsonianone A, isolated from the fruit of Rhodomyrtus tomentosa (Ait.) Hassk, was found to show a good inhibitory effect on RSV-induced NO production, with a half-maximal inhibitory concentration of 37.2 ± 1.6 µM. Enzyme-linked immunosorbent assay and fluorescence quantitative polymerase chain reaction analyses indicated that watsonianone A markedly reduced both mRNA and protein levels of tumor necrosis factor α, interleukin 6, and monocyte chemoattractant protein 1 in RSV-infected RAW264.7 cells. Mechanistically, watsonianone A inhibited nuclear factor κB (NF-κB) activation by suppressing IκBα phosphorylation. Further analysis revealed that watsonianone A activated the thioredoxin system and decreased intracellular reactive oxygen species (ROS) levels, which are closely associated with NF-κB activation in RSV-infected cells. These results reveal that watsonianone A can attenuate RSV-induced inflammation via the suppression of ROS-sensitive inflammatory signaling.
[Mh] Termos MeSH primário: Cicloexanonas/farmacologia
Frutas/química
Myrtaceae/química
Extratos Vegetais/farmacologia
Infecções por Vírus Respiratório Sincicial/imunologia
Vírus Sinciciais Respiratórios/efeitos dos fármacos
[Mh] Termos MeSH secundário: Seres Humanos
Proteínas I-kappa B/genética
Proteínas I-kappa B/imunologia
Interleucina-6/genética
Interleucina-6/imunologia
NF-kappa B/genética
NF-kappa B/imunologia
Espécies Reativas de Oxigênio/imunologia
Infecções por Vírus Respiratório Sincicial/tratamento farmacológico
Infecções por Vírus Respiratório Sincicial/virologia
Vírus Sinciciais Respiratórios/fisiologia
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclohexanones); 0 (I-kappa B Proteins); 0 (IL6 protein, human); 0 (Interleukin-6); 0 (NF-kappa B); 0 (Plant Extracts); 0 (Reactive Oxygen Species); 0 (Tumor Necrosis Factor-alpha); 0 (watsonianone A)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170608
[Lr] Data última revisão:
170608
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170425
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jafc.7b00537



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