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Pesquisa : D12.644.360.024.313 [Categoria DeCS]
Referências encontradas : 207 [refinar]
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[PMID]:28783736
[Au] Autor:Kang P; Wang X; Wu H; Zhu H; Hou Y; Wang L; Liu Y
[Ad] Endereço:Hubei Collaborative Innovation Center for Animal Nutrition and Feed Safety, Hubei Key Laboratory of Animal Nutrition and Feed Science, Wuhan Polytechnic University, Wuhan, People's Republic of China.
[Ti] Título:Glutamate alleviates muscle protein loss by modulating TLR4, NODs, Akt/FOXO and mTOR signaling pathways in LPS-challenged piglets.
[So] Source:PLoS One;12(8):e0182246, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The experiment was conducted to study the effect of the glutamate (Glu) on muscle protein loss through toll-like receptor 4 (TLR4), nucleotide-binding oligomerization domain proteins (NODs), Akt/Forkhead Box O (Akt/FOXO) and mammalian target of rapamycin (mTOR) signaling pathways in LPS-challenged piglets. Twenty-four weaned piglets were assigned into four treatments: (1) Control; (2) LPS+0% Glu; (3) LPS + 1.0% Glu; (4) LPS + 2.0% Glu. The experiment was lasted for 28 days. On d 28, the piglets in the LPS challenged groups were injected with LPS on 100 µg/kg body weight (BW), and the piglets in the control group were injected with the same volume of 0.9% NaCl solution. After 4 h LPS or saline injection, the piglets were slaughtered and the muscle samples were collected. Glu supplementation increased the protein/DNA ratio in gastrocnemius muscle, and the protein content in longissimus dorsi (LD) muscle after LPS challenge (P<0.05). In addition, Glu supplementation decreased TLR4, IL-1 receptor-associated kinase (IRAK) 1, receptor-interacting serine/threonine-protein kinase (RIPK) 2, and nuclear factor-κB (NF-κB) mRNA expression in gastrocnemius muscle (P<0.05), MyD88 mRNA expression in LD muscle, and FOXO1 mRNA expression in LD muscle (P<0.05). Moreover, Glu supplementation increased p-Akt/t-Akt ratio (P<0.05) in gastrocnemius muscle, and p-4EBP1/t-4EBP1 ratio in both gastrocnemius and LD muscles (P<0.05). Glu supplementation in the piglets' diets might be an effective strategy to alleviate LPS-induced muscle protein loss, which might be due to suppressing the mRNA expression of TLR4 and NODs signaling-related genes, and modulating Akt/FOXO and mTOR signaling pathways.
[Mh] Termos MeSH primário: Ácido Glutâmico/farmacologia
Lipopolissacarídeos/farmacologia
Proteínas Musculares/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
DNA/metabolismo
Fatores de Transcrição Forkhead/genética
Fatores de Transcrição Forkhead/metabolismo
Regulação da Expressão Gênica/efeitos dos fármacos
Proteínas Musculares/genética
Músculo Esquelético/citologia
Músculo Esquelético/efeitos dos fármacos
Músculo Esquelético/metabolismo
Proteínas Adaptadoras de Sinalização NOD/genética
Proteínas Adaptadoras de Sinalização NOD/metabolismo
Fosfoproteínas/genética
Fosfoproteínas/metabolismo
Proteínas Proto-Oncogênicas c-akt/genética
Proteínas Proto-Oncogênicas c-akt/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Suínos
Serina-Treonina Quinases TOR/genética
Serina-Treonina Quinases TOR/metabolismo
Receptor 4 Toll-Like/genética
Receptor 4 Toll-Like/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Forkhead Transcription Factors); 0 (Lipopolysaccharides); 0 (Muscle Proteins); 0 (Nod Signaling Adaptor Proteins); 0 (Phosphoproteins); 0 (RNA, Messenger); 0 (Toll-Like Receptor 4); 3KX376GY7L (Glutamic Acid); 9007-49-2 (DNA); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[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:170808
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0182246


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[PMID]:28029143
[Au] Autor:Zhang Z; Wang X; Zheng G; Shan Q; Lu J; Fan S; Sun C; Wu D; Zhang C; Su W; Sui J; Zheng Y
[Ad] Endereço:Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou 221116, China. zhangzifengsuper@jsnu.edu.cn.
[Ti] Título:Troxerutin Attenuates Enhancement of Hepatic Gluconeogenesis by Inhibiting NOD Activation-Mediated Inflammation in High-Fat Diet-Treated Mice.
[So] Source:Int J Mol Sci;18(1), 2016 Dec 25.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Recent evidence suggests that troxerutin, a trihydroxyethylated derivative of natural bioflavonoid rutin, exhibits beneficial effects on diabetes-related symptoms. Here we investigated the effects of troxerutin on the enhancement of hepatic gluconeogenesis in high-fat diet (HFD)-treated mice and the mechanisms underlying these effects. Mice were divided into four groups: Control group, HFD group, HFD + Troxerutin group, and Troxerutin group. Troxerutin was treated by daily oral administration at doses of 150 mg/kg/day for 20 weeks. Tauroursodeoxycholic acid (TUDCA) was used to inhibit endoplasmic reticulum stress (ER stress). Our results showed that troxerutin effectively improved obesity and related metabolic parameters, and liver injuries in HFD-treated mouse. Furthermore, troxerutin significantly attenuated enhancement of hepatic gluconeogenesis in HFD-fed mouse. Moreover, troxerutin notably suppressed nuclear factor-κB (NF-κB) p65 transcriptional activation and release of inflammatory cytokines in HFD-treated mouse livers. Mechanismly, troxerutin dramatically decreased Nucleotide oligomerization domain (NOD) expression, as well as interaction between NOD1/2 with interacting protein-2 (RIP2), by abating oxidative stress-induced ER stress in HFD-treated mouse livers, which was confirmed by TUDCA treatment. These improvement effects of troxerutin on hepatic glucose disorders might be mediated by its anti-obesity effect. In conclusion, troxerutin markedly diminished HFD-induced enhancement of hepatic gluconeogenesis via its inhibitory effects on ER stress-mediated NOD activation and consequent inflammation, which might be mediated by its anti-obesity effect.
[Mh] Termos MeSH primário: Anti-Inflamatórios/farmacologia
Gluconeogênese
Hidroxietilrutosídeo/análogos & derivados
Hiperglicemia/metabolismo
Fígado/metabolismo
Proteínas Adaptadoras de Sinalização NOD/metabolismo
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios/administração & dosagem
Anti-Inflamatórios/uso terapêutico
Dieta Hiperlipídica/efeitos adversos
Estresse do Retículo Endoplasmático
Hidroxietilrutosídeo/administração & dosagem
Hidroxietilrutosídeo/farmacologia
Hidroxietilrutosídeo/uso terapêutico
Hiperglicemia/tratamento farmacológico
Hiperglicemia/etiologia
Fígado/efeitos dos fármacos
Masculino
Camundongos
Camundongos Endogâmicos ICR
NF-kappa B/genética
NF-kappa B/metabolismo
Estresse Oxidativo
Proteína Serina-Treonina Quinases de Interação com Receptores/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Hydroxyethylrutoside); 0 (NF-kappa B); 0 (Nod Signaling Adaptor Proteins); 7Y4N11PXO8 (troxerutin); EC 2.7.11.1 (Receptor-Interacting Protein Serine-Threonine Kinases); EC 2.7.11.1 (Ripk2 protein, mouse)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170406
[Lr] Data última revisão:
170406
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161229
[St] Status:MEDLINE


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[PMID]:27572423
[Au] Autor:Wang X; Liu Y; Wang S; Pi D; Leng W; Zhu H; Zhang J; Shi H; Li S; Lin X; Odle J
[Ad] Endereço:1Hubei Key Laboratory of Animal Nutrition and Feed Science,Hubei Collaborative Innovation Center for Animal Nutrition and Feed Safety,Wuhan Polytechnic University,Wuhan 430023,People's Republic of China.
[Ti] Título:Asparagine reduces the mRNA expression of muscle atrophy markers via regulating protein kinase B (Akt), AMP-activated protein kinase α, toll-like receptor 4 and nucleotide-binding oligomerisation domain protein signalling in weaning piglets after lipopolysaccharide challenge.
[So] Source:Br J Nutr;116(7):1188-1198, 2016 Oct.
[Is] ISSN:1475-2662
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Pro-inflammatory cytokines are critical in mechanisms of muscle atrophy. In addition, asparagine (Asn) is necessary for protein synthesis in mammalian cells. We hypothesised that Asn could attenuate lipopolysaccharide (LPS)-induced muscle atrophy in a piglet model. Piglets were allotted to four treatments (non-challenged control, LPS-challenged control, LPS+0·5 % Asn and LPS+1·0 % Asn). On day 21, the piglets were injected with LPS or saline. At 4 h post injection, piglet blood and muscle samples were collected. Asn increased protein and RNA content in muscles, and decreased mRNA expression of muscle atrophy F-box (MAFbx) and muscle RING finger 1 (MuRF1). However, Asn had no effect on the protein abundance of MAFbx and MuRF1. In addition, Asn decreased muscle AMP-activated protein kinase (AMPK) α phosphorylation, but increased muscle protein kinase B (Akt) and Forkhead Box O (FOXO) 1 phosphorylation. Moreover, Asn decreased the concentrations of TNF-α, cortisol and glucagon in plasma, and TNF-α mRNA expression in muscles. Finally, Asn decreased mRNA abundance of muscle toll-like receptor (TLR) 4 and nucleotide-binding oligomerisation domain protein (NOD) signalling-related genes, and regulated their negative regulators. The beneficial effects of Asn on muscle atrophy may be associated with the following: (1) inhibiting muscle protein degradation via activating Akt and inactivating AMPKα and FOXO1; and (2) decreasing the expression of muscle pro-inflammatory cytokines via inhibiting TLR4 and NOD signalling pathways by modulation of their negative regulators.
[Mh] Termos MeSH primário: Proteínas Quinases Ativadas por AMP/metabolismo
Asparagina/farmacologia
Expressão Gênica/efeitos dos fármacos
Atrofia Muscular/genética
Proteínas Proto-Oncogênicas c-akt/metabolismo
Receptor 4 Toll-Like/metabolismo
[Mh] Termos MeSH secundário: Proteínas Quinases Ativadas por AMP/antagonistas & inibidores
Animais
Ativação Enzimática/efeitos dos fármacos
Proteínas F-Box/análise
Proteínas F-Box/genética
Proteína Forkhead Box O1/antagonistas & inibidores
Lipopolissacarídeos/farmacologia
Proteínas Musculares/metabolismo
Músculo Esquelético/química
Atrofia Muscular/induzido quimicamente
Proteínas Adaptadoras de Sinalização NOD/antagonistas & inibidores
Fosforilação/efeitos dos fármacos
Complexo Repressor Polycomb 1/análise
Complexo Repressor Polycomb 1/genética
RNA Mensageiro/análise
Transdução de Sinais/efeitos dos fármacos
Sus scrofa
Receptor 4 Toll-Like/genética
Desmame
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (F-Box Proteins); 0 (Forkhead Box Protein O1); 0 (Lipopolysaccharides); 0 (Muscle Proteins); 0 (Nod Signaling Adaptor Proteins); 0 (RNA, Messenger); 0 (Toll-Like Receptor 4); 7006-34-0 (Asparagine); EC 2.3.2.27 (Polycomb Repressive Complex 1); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 2.7.11.31 (AMP-Activated Protein Kinases)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160831
[St] Status:MEDLINE


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[PMID]:27122187
[Au] Autor:Wang D; Chen J; Li R; Wu G; Sun Z; Wang Z; Zhai Z; Fang F; Guo Y; Zhong Y; Jiang M; Xu H; Chen M; Shen G; Sun J; Yan B; Yu C; Tian Z; Xiao W
[Ad] Endereço:Key Laboratory of Innate Immunity and Chronic Disease of CAS, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230027, China Hefei National Laboratory for Physical Sciences at Microscale, Hefei, Anhui 230027, China Innovation Center for Cell Signaling Network, Sch
[Ti] Título:PAX5 interacts with RIP2 to promote NF-κB activation and drug-resistance in B-lymphoproliferative disorders.
[So] Source:J Cell Sci;129(11):2261-72, 2016 06 01.
[Is] ISSN:1477-9137
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Paired box protein 5 (PAX5) plays a lineage determination role in B-cell development. However, high expression of PAX5 has been also found in various malignant diseases, including B-lymphoproliferative disorders (B-LPDs), but its functions and mechanisms in these diseases are still unclear. Here, we show that PAX5 induces drug resistance through association and activation of receptor-interacting serine/threonine-protein kinase 2 (RIP2; also known as RIPK2), and subsequent activation of NF-κB signaling and anti-apoptosis gene expression in B-lymphoproliferative cells. Furthermore, PAX5 is able to interact with RIP1 and RIP3, modulating both RIP1-mediated TNFR and RIP2-mediated NOD1 and NOD2 pathways. Our findings describe a new function of PAX5 in regulating RIP1 and RIP2 activation, which is at least involved in chemotherapeutic drug resistance in B-LPDs.
[Mh] Termos MeSH primário: Linfócitos B/metabolismo
Resistência a Medicamentos Antineoplásicos
Transtornos Linfoproliferativos/metabolismo
NF-kappa B/metabolismo
Fator de Transcrição PAX5/metabolismo
Proteína Serina-Treonina Quinase 2 de Interação com Receptor/metabolismo
[Mh] Termos MeSH secundário: Antineoplásicos/farmacologia
Antineoplásicos/uso terapêutico
Linfócitos B/efeitos dos fármacos
Bortezomib/farmacologia
Bortezomib/uso terapêutico
Carcinogênese/metabolismo
Carcinogênese/patologia
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Resistência a Medicamentos Antineoplásicos/efeitos dos fármacos
Seres Humanos
Transtornos Linfoproliferativos/patologia
Modelos Biológicos
Proteínas Adaptadoras de Sinalização NOD/metabolismo
Ligação Proteica/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
Fator de Necrose Tumoral alfa/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (NF-kappa B); 0 (Nod Signaling Adaptor Proteins); 0 (PAX5 Transcription Factor); 0 (Tumor Necrosis Factor-alpha); 69G8BD63PP (Bortezomib); EC 2.7.11.1 (RIPK2 protein, human); EC 2.7.11.1 (Receptor-Interacting Protein Serine-Threonine Kinase 2)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171124
[Lr] Data última revisão:
171124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160429
[St] Status:MEDLINE
[do] DOI:10.1242/jcs.183889


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[PMID]:26979266
[Au] Autor:Li J; Chu Q; Xu T
[Ad] Endereço:Laboratory of Fish Biogenetics & Immune Evolution, College of Marine Science, Zhejiang Ocean University, Zhoushan, 316022, China.
[Ti] Título:A genome-wide survey of expansive NLR-C subfamily in miiuy croaker and characterization of the NLR-B30.2 genes.
[So] Source:Dev Comp Immunol;61:116-25, 2016 08.
[Is] ISSN:1879-0089
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:NOD-like receptors (NLRs) are essential intracellular pattern-recognition receptors that respond to pathogens and regulate innate immunity. NLRs include three distinct subfamilies: NLR-A, NLR-B and NLR-C, thereinto, NLR-C as a large subfamily is unique to bony fish and little research about it has been done. In the current study, we identified the members of NLR-B and NLR-C subfamilies containing 2 and 48 genes respectively in miiuy croaker. Compared with other teleosts except for zebrafish, NLR-C subfamily genes occurred expansion in miiuy croaker. The gene expansions of NLR-C subfamily may illustrate adaptive genome evolution in response to specific aquatic environments. Structural analysis showed that the N-terminus of NLR-C subfamily receptors has different characteristics of the domains including RING domain, FISNA domain or PYRIN domain. Interestingly, the C-terminus of 18 NLR-C subfamily members contains an extra B30.2 domain (named NLR-B30.2 genes) which plays an important role in antiviral immune recognition. Simultaneously, molecular evolutionary analysis indicated that the positively sites in miiuy croaker are mainly located in NACHT domain which was the vital region for signal transduction in immune response. Significantly, pathogens challenge in spleen and macrophages demonstrated that NLR-B30.2 genes exhibited more sensitive response to virus than bacteria, suggesting these genes play enhanced roles in innate antiviral immunity, which may represent a new family used for antiviral infection.
[Mh] Termos MeSH primário: Infecções Bacterianas/imunologia
Genoma
Macrófagos/imunologia
Proteínas NLR/metabolismo
Proteínas Adaptadoras de Sinalização NOD/metabolismo
Perciformes/imunologia
Viroses/imunologia
[Mh] Termos MeSH secundário: Animais
Proteínas Reguladoras de Apoptose/metabolismo
Infecções Bacterianas/genética
Células Cultivadas
Evolução Molecular
Imunidade Inata/genética
Família Multigênica/genética
Proteínas NLR/genética
Proteínas Adaptadoras de Sinalização NOD/genética
Filogenia
Transdução de Sinais
Viroses/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Apoptosis Regulatory Proteins); 0 (NLR Proteins); 0 (Nod Signaling Adaptor Proteins)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171120
[Lr] Data última revisão:
171120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160317
[St] Status:MEDLINE


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[PMID]:26836127
[Au] Autor:Calcaterra R; Di Girolamo M; Mirisola C; Baggi L
[Ad] Endereço:*Researcher, Department of Social Dentistry, National Institute for Health, Migration and Poverty, Rome, Italy. †Assistant Professor, Department of Clinical Sciences and Translational Research, School of Dentistry, University of Rome, Torvergata, Italy. ‡Director, Department of General Direction, National Institute for Health, Migration, and Poverty, Rome, Italy. §Director, Department of Social Dentistry, National Institute for Health, Migration and Poverty-Associate Professor School of Dentistry, University of Rome Tor vergata, Italy.
[Ti] Título:Expression of Pattern Recognition Receptors in Epithelial Cells Around Clinically Healthy Implants and Healthy Teeth.
[So] Source:Implant Dent;25(3):348-52, 2016 Jun.
[Is] ISSN:1538-2982
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Gingival epithelial cells have a pivotal role in the recognition of microorganisms and damage-associated molecular pattern molecules and in the regulation of the immune response. The investigation of the behavior of Toll-like receptors (TLRs) and nucleotide oligomerization domain (NOD) like receptors (NLRs) around a healthy implant may help to address the first step of periimplantitis pathogenesis. PURPOSE: To investigate by quantitative real-time polymerase chain reaction, the mRNA expressions of TLR2, TLR3, TLR4, TLR5, TLR6, TLR9, NOD1, NOD2, and NLRP3 from gingival epithelial cells of the sulcus around healthy implants and around healthy teeth. MATERIALS AND METHODS: Two types of implant-abutment systems with tube-in-tube interface were tested. After 6 months of implant restoration, gingival epithelial cells were obtained from the gingival sulcus around the implants and around the adjacent teeth of 10 patients. RESULTS: Our results did not reach statistical significance among the mRNA expressions of TLR2, TLR3, TLR4, TLR5, TLR6, TLR9, NOD1, NOD2, and NLRP3 in epithelial cells around the implant versus around natural teeth. CONCLUSION: This study shows that the implant-abutment systems tested did not induce an immune response by the surrounding epithelial cells at 6 months since their positioning, as well as in the adjacent clincally healthy teeth.
[Mh] Termos MeSH primário: Implantes Dentários
Epitélio/metabolismo
Gengiva/citologia
Proteínas Adaptadoras de Sinalização NOD/metabolismo
Receptores Toll-Like/metabolismo
[Mh] Termos MeSH secundário: Implantes Dentários/efeitos adversos
Gengiva/metabolismo
Seres Humanos
Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo
Proteína Adaptadora de Sinalização NOD1/metabolismo
Proteína Adaptadora de Sinalização NOD2/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Receptor 2 Toll-Like/metabolismo
Receptor 3 Toll-Like/metabolismo
Receptor 4 Toll-Like/metabolismo
Receptor 5 Toll-Like/metabolismo
Receptor 6 Toll-Like/metabolismo
Receptor Toll-Like 9/metabolismo
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dental Implants); 0 (NLR Family, Pyrin Domain-Containing 3 Protein); 0 (NLRP3 protein, human); 0 (NOD1 protein, human); 0 (NOD2 protein, human); 0 (Nod Signaling Adaptor Proteins); 0 (Nod1 Signaling Adaptor Protein); 0 (Nod2 Signaling Adaptor Protein); 0 (TLR2 protein, human); 0 (TLR3 protein, human); 0 (TLR4 protein, human); 0 (TLR5 protein, human); 0 (TLR6 protein, human); 0 (TLR9 protein, human); 0 (Toll-Like Receptor 2); 0 (Toll-Like Receptor 3); 0 (Toll-Like Receptor 4); 0 (Toll-Like Receptor 5); 0 (Toll-Like Receptor 6); 0 (Toll-Like Receptor 9); 0 (Toll-Like Receptors)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170601
[Lr] Data última revisão:
170601
[Sb] Subgrupo de revista:D
[Da] Data de entrada para processamento:160203
[St] Status:MEDLINE
[do] DOI:10.1097/ID.0000000000000379


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[PMID]:26833430
[Au] Autor:Li L; Yu H; Jiang Y; Deng B; Bai L; Kijlstra A; Yang P
[Ad] Endereço:The First Affiliated Hospital of Chongqing Medical University, Chongqing Key Laboratory of Ophthalmology, and Chongqing Eye Institute, Chongqing, P R China.
[Ti] Título:Genetic Variations of NLR family genes in Behcet's Disease.
[So] Source:Sci Rep;6:20098, 2016 Feb 01.
[Is] ISSN:2045-2322
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:This study aimed to investigate whether single nucleotide polymorphisms (SNPs) of five NLR family genes (NOD1, NOD2, NLRP1, NLRP3 and CIITA) are associated with Behcet's disease (BD) in a Chinese Han population. The study was carried out in 950 BD patients and 1440 controls for 19 SNPs in the selected NLR genes. In the first-stage study, significantly decreased frequencies of the CIITA//rs12932187 C allele (Pc = 1.668E-02) and NOD1//rs2075818 G allele (Pc = 4.694E-02) were found in BD patients as compared to controls . After performing a second stage validation study and combination of data we confirmed the association of CIITA//rs12932187 and NOD1//rs2075818 with BD. In CIITA//rs12932187, the frequencies of the CC genotype and C allele were significantly lower in BD than in controls (Pc = 3.331E-06; Pc = 6.004E-07, respectively). In NOD1//rs2075818, the GG genotype and G allele showed significantly decreased frequencies in BD patients when compared to controls (Pc = 1.022E-02; Pc = 6.811E-05, respectively). Functional experiments showed that carriers with the CC genotype in CIITA//rs12932187 had a lower CIITA mRNA expression level and an enhanced IL-10 secretion as compared to GG and CG carriers. This study provides evidence that the CIITA and NOD1 gene are involved in the susceptibility to Behcet's disease.
[Mh] Termos MeSH primário: Alelos
Síndrome de Behçet/genética
Frequência do Gene
Genótipo
Proteínas Adaptadoras de Sinalização NOD/genética
Polimorfismo de Nucleotídeo Único
[Mh] Termos MeSH secundário: Grupo com Ancestrais do Continente Asiático
China
Feminino
Seres Humanos
Masculino
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE; MULTICENTER STUDY; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Nod Signaling Adaptor Proteins)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160203
[St] Status:MEDLINE
[do] DOI:10.1038/srep20098


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[PMID]:26814423
[Au] Autor:Shiny A; Regin B; Mohan V; Balasubramanyam M
[Ad] Endereço:Department of Cell and Molecular Biology, Madras Diabetes Research Foundation, Dr. Mohan's Diabetes Specialities Centre Gopalapuram, Chennai, India. Electronic address: shinyabhijit@gmail.com.
[Ti] Título:Coordinated augmentation of NFAT and NOD signaling mediates proliferative VSMC phenotype switch under hyperinsulinemia.
[So] Source:Atherosclerosis;246:257-66, 2016 Mar.
[Is] ISSN:1879-1484
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:AIM: Although hyperglycemia has been demonstrated to play a significant role in the vascular disease associated with type 2 diabetes, the mechanisms underlying hyperinsulinemia mediated vascular dysfunction are not well understood. We have analyzed whether hyperinsulinemia could activate NFAT (Nuclear factor of activated T cells) signaling and thereby influence vascular smooth muscle cell (VSMC) migration and proliferation, a major event in the progression of atherosclerosis. METHODS AND RESULTS: Human aortic VSMCs upon chronic insulin treatment exhibited increased expression of NFATc1 both at the mRNA and protein levels. The mechanistic role of NFAT in VSMC migration and proliferation was examined using 11R-VIVIT, a cell permeable NFAT specific inhibitor, where it reduced the insulin effect on VSMC, which was further substantiated by over expression or silencing of NFATc1gene (p < 0.05). This study also report for the first time the role of NFAT in NOD (Nucleotide oligomerization domain) mediated innate immune signaling and its significance in insulin effect on VSMCs. mRNA expression of NOD was up regulated when cells were treated with insulin or ligands whereas pretreatment with 11R-VIVIT reversed this effect (p < 0.05). Our study uphold the clinical significance as we observed an increased mRNA expression of NFATc1 in monocytes isolated from patients with type 2 diabetes which correlated positively with insulin resistance and glycemic load (p < 0.05). DISCUSSION: This study suggests that targeted NFAT inhibition can be an effective strategy to coordinately quench insulin induced proliferative and inflammatory responses along with innate immunity alterations in vascular smooth muscle cells, which underlie atherosclerosis.
[Mh] Termos MeSH primário: Aterosclerose/metabolismo
Proliferação Celular
Diabetes Mellitus Tipo 2/metabolismo
Angiopatias Diabéticas/metabolismo
Hiperinsulinismo/metabolismo
Músculo Liso Vascular/metabolismo
Miócitos de Músculo Liso/metabolismo
Fatores de Transcrição NFATC/metabolismo
Proteínas Adaptadoras de Sinalização NOD/metabolismo
[Mh] Termos MeSH secundário: Aterosclerose/genética
Aterosclerose/patologia
Glicemia/metabolismo
Linhagem Celular
Movimento Celular
Proliferação Celular/efeitos dos fármacos
Diabetes Mellitus Tipo 2/genética
Diabetes Mellitus Tipo 2/patologia
Angiopatias Diabéticas/genética
Angiopatias Diabéticas/patologia
Seres Humanos
Hiperinsulinismo/genética
Hiperinsulinismo/patologia
Imunidade Inata
Insulina/metabolismo
Resistência à Insulina
Músculo Liso Vascular/efeitos dos fármacos
Músculo Liso Vascular/patologia
Miócitos de Músculo Liso/efeitos dos fármacos
Miócitos de Músculo Liso/patologia
Fatores de Transcrição NFATC/antagonistas & inibidores
Fatores de Transcrição NFATC/genética
Proteínas Adaptadoras de Sinalização NOD/genética
Proteína Adaptadora de Sinalização NOD1/metabolismo
Proteína Adaptadora de Sinalização NOD2/metabolismo
Oligopeptídeos/farmacologia
Interferência de RNA
Transdução de Sinais
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Insulin); 0 (NFATC Transcription Factors); 0 (NFATC1 protein, human); 0 (NOD1 protein, human); 0 (NOD2 protein, human); 0 (Nod Signaling Adaptor Proteins); 0 (Nod1 Signaling Adaptor Protein); 0 (Nod2 Signaling Adaptor Protein); 0 (Oligopeptides); 0 (VIVIT peptide)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160128
[St] Status:MEDLINE


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[PMID]:26636731
[Au] Autor:Via VD; Zanetti ME; Blanco F
[Ad] Endereço:a Instituto de Biotecnología y Biología Molecular, Facultad de Ciencias Exactas, Universidad Nacional de La Plata, CCT-La Plata, CONICET , La Plata , Argentina.
[Ti] Título:How legumes recognize rhizobia.
[So] Source:Plant Signal Behav;11(2):e1120396, 2016.
[Is] ISSN:1559-2324
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Legume plants have developed the capacity to establish symbiotic interactions with soil bacteria (known as rhizobia) that can convert N2 to molecular forms that are incorporated into the plant metabolism. The first step of this relationship is the recognition of bacteria by the plant, which allows to distinguish potentially harmful species from symbiotic partners. The main molecular determinant of this symbiotic interaction is the Nod Factor, a diffusible lipochitooligosaccharide molecule produced by rhizobia and perceived by LysM receptor kinases; however, other important molecules involved in the specific recognition have emerged over the years. Secreted exopolysaccharides and the lipopolysaccharides present in the bacterial cell wall have been proposed to act as signaling molecules, triggering the expression of specific genes related to the symbiotic process. In this review we will briefly discuss how transcriptomic analysis are helping to understand how multiple signaling pathways, triggered by the perception of different molecules produced by rhizobia, control the genetic programs of root nodule organogenesis and bacterial infection. This knowledge can help to understand how legumes have evolved to recognize and establish complex ecological relationships with particular species and strains of rhizobia, adjusting gene expression in response to identity determinants of bacteria.
[Mh] Termos MeSH primário: Fabaceae/microbiologia
Modelos Biológicos
Rhizobiaceae/metabolismo
Transdução de Sinais
Simbiose/fisiologia
[Mh] Termos MeSH secundário: Fabaceae/genética
Fabaceae/metabolismo
Proteínas Fúngicas/química
Proteínas Fúngicas/metabolismo
Proteínas Adaptadoras de Sinalização NOD/química
Proteínas Adaptadoras de Sinalização NOD/metabolismo
Proteínas Adaptadoras de Sinalização NOD/fisiologia
Proteínas de Plantas/química
Proteínas de Plantas/genética
Proteínas de Plantas/metabolismo
Nódulos Radiculares de Plantas/genética
Nódulos Radiculares de Plantas/metabolismo
Nódulos Radiculares de Plantas/microbiologia
Especificidade da Espécie
Simbiose/genética
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Fungal Proteins); 0 (Nod Signaling Adaptor Proteins); 0 (Plant Proteins)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151205
[St] Status:MEDLINE
[do] DOI:10.1080/15592324.2015.1120396


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[PMID]:26632377
[Au] Autor:Kim YK; Shin JS; Nahm MH
[Ad] Endereço:Department of Internal Medicine, Yonsei University Wonju College of Medicine, Wonju, Korea.
[Ti] Título:NOD-Like Receptors in Infection, Immunity, and Diseases.
[So] Source:Yonsei Med J;57(1):5-14, 2016 Jan.
[Is] ISSN:1976-2437
[Cp] País de publicação:Korea (South)
[La] Idioma:eng
[Ab] Resumo:Nucleotide-binding and oligomerization domain (NOD)-like receptors (NLRs) are pattern-recognition receptors similar to toll-like receptors (TLRs). While TLRs are transmembrane receptors, NLRs are cytoplasmic receptors that play a crucial role in the innate immune response by recognizing pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). Based on their N-terminal domain, NLRs are divided into four subfamilies: NLRA, NLRB, NLRC, and NLRP. NLRs can also be divided into four broad functional categories: inflammasome assembly, signaling transduction, transcription activation, and autophagy. In addition to recognizing PAMPs and DAMPs, NLRs act as a key regulator of apoptosis and early development. Therefore, there are significant associations between NLRs and various diseases related to infection and immunity. NLR studies have recently begun to unveil the roles of NLRs in diseases such as gout, cryopyrin-associated periodic fever syndromes, and Crohn's disease. As these new associations between NRLs and diseases may improve our understanding of disease pathogenesis and lead to new approaches for the prevention and treatment of such diseases, NLRs are becoming increasingly relevant to clinicians. In this review, we provide a concise overview of NLRs and their role in infection, immunity, and disease, particularly from clinical perspectives.
[Mh] Termos MeSH primário: Imunidade Inata
Proteínas Adaptadoras de Sinalização NOD/metabolismo
Receptores Citoplasmáticos e Nucleares/metabolismo
Receptores de Reconhecimento de Padrão/imunologia
Transdução de Sinais
[Mh] Termos MeSH secundário: Autofagia/imunologia
Proteínas de Transporte
Seres Humanos
Inflamassomos
Proteínas Adaptadoras de Sinalização NOD/imunologia
Padrões Moleculares Associados a Patógenos
Receptores Citoplasmáticos e Nucleares/imunologia
Receptores Toll-Like/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Carrier Proteins); 0 (Inflammasomes); 0 (Nod Signaling Adaptor Proteins); 0 (Pathogen-Associated Molecular Pattern Molecules); 0 (Receptors, Cytoplasmic and Nuclear); 0 (Receptors, Pattern Recognition); 0 (Toll-Like Receptors)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151204
[St] Status:MEDLINE
[do] DOI:10.3349/ymj.2016.57.1.5



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