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  1 / 3005 MEDLINE  
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[PMID]:29421442
[Au] Autor:Wu S; Mao L; Li Y; Yin Y; Yuan W; Chen Y; Ren W; Lu X; Li Y; Chen L; Chen B; Xu W; Tian T; Lu Y; Jiang L; Zhuang X; Chu M; Wu J
[Ad] Endereço:Jiangsu Provincial Key Laboratory of Geriatrics, Department of Geriatrics, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
[Ti] Título:RAGE may act as a tumour suppressor to regulate lung cancer development.
[So] Source:Gene;651:86-93, 2018 Apr 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Although the correlation of the RAGE rs2070600 polymorphism and cancer risk has been confirmed, detailed studies with functional and experimental evaluations are lacking. In this study, we first aimed to examine whether this polymorphism is associated with cancer risk based on the latest published data, and consistent with previous meta-analyses, a significant association between the rs2070600 polymorphism and cancer risk was observed (A versus G: OR = 1.25; 95% CI = 1.12-1.40). In additional stratified analyses based on cancer type, rs2070600 was significantly associated with an increased risk of lung cancer (A versus G: OR = 1.20; 95% CI = 1.09-1.33). Moreover, TCGA database showed that the expression level of RAGE was significantly lower in lung cancer tumour tissues than in adjacent non-tumour tissues, which was validated in the GEO database. Additionally, eQTL analysis indicated that the rs2070600 polymorphism may modify the expression level of RAGE in lung squamous cell carcinoma tissues (P = 0.09). Finally, we performed functional experiments in lung cancer cells and preliminarily demonstrated that RAGE may act as a tumour suppressor in lung cancer development. These findings provide evidence that the variant A allele of rs2070600 may decrease the expression of the tumour suppressor gene RAGE, thereby increasing lung cancer risk.
[Mh] Termos MeSH primário: Genes Supressores de Tumor
Neoplasias Pulmonares/genética
Polimorfismo de Nucleotídeo Único
Receptor para Produtos Finais de Glicação Avançada/genética
[Mh] Termos MeSH secundário: Linhagem Celular
Linhagem Celular Tumoral
Expressão Gênica
Predisposição Genética para Doença
Seres Humanos
Neoplasias Pulmonares/patologia
Fenótipo
Locos de Características Quantitativas
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS
[Nm] Nome de substância:
0 (Receptor for Advanced Glycation End Products)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180209
[St] Status:MEDLINE


  2 / 3005 MEDLINE  
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[PMID]:29394248
[Au] Autor:Srinivasan L; Kilpatrick L; Shah SS; Abbasi S; Harris MC
[Ad] Endereço:Department of Pediatrics, The Children's Hospital of Philadelphia, Philadelphia, PA, United States of America.
[Ti] Título:Elevations of novel cytokines in bacterial meningitis in infants.
[So] Source:PLoS One;13(2):e0181449, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Bacterial meningitis is challenging to diagnose in infants, especially in the common setting of antibiotic pre-treatment, which diminishes yield of cerebrospinal fluid (CSF) cultures. Prior studies of diagnostic markers have not demonstrated sufficient accuracy. Interleukin-23 (IL-23), interleukin-18 (IL-18) and soluble receptor for advanced glycation end products (sRAGE) possess biologic plausibility, and may be useful as diagnostic markers in bacterial meningitis. METHODS: In a prospective cohort study, we measured IL-23, IL-18 and sRAGE levels in CSF. We compared differences between infected and non-infected infants, and conducted receiver operating characteristic (ROC) analyses to identify individual markers and combinations of markers with the best diagnostic accuracy. RESULTS: 189 infants <6 months, including 8 with bacterial meningitis, 30 without meningitis, and 151 with indeterminate diagnosis (due to antibiotic pretreatment) were included. CSF IL-23, IL-18 and sRAGE levels were significantly elevated in infants with culture proven meningitis. Among individual markers, IL-23 possessed the greatest accuracy for diagnosis of bacterial meningitis (area under the curve (AUC) 0.9698). The combination of all three markers had an AUC of 1. CONCLUSIONS: IL-23, alone and in combination with IL-18 and sRAGE, identified bacterial meningitis with excellent accuracy. Following validation, these markers could aid clinicians in diagnosis of bacterial meningitis and decision-making regarding prolongation of antibiotic therapy.
[Mh] Termos MeSH primário: Citocinas/líquido cefalorraquidiano
Meningites Bacterianas/líquido cefalorraquidiano
[Mh] Termos MeSH secundário: Biomarcadores/líquido cefalorraquidiano
Feminino
Seres Humanos
Lactente
Recém-Nascido
Interleucina-18/líquido cefalorraquidiano
Interleucina-23/líquido cefalorraquidiano
Masculino
Estudos Prospectivos
Receptor para Produtos Finais de Glicação Avançada/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers); 0 (Cytokines); 0 (Interleukin-18); 0 (Interleukin-23); 0 (Receptor for Advanced Glycation End Products)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180203
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0181449


  3 / 3005 MEDLINE  
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[PMID]:29191879
[Au] Autor:Engblom C; Pfirschke C; Zilionis R; Da Silva Martins J; Bos SA; Courties G; Rickelt S; Severe N; Baryawno N; Faget J; Savova V; Zemmour D; Kline J; Siwicki M; Garris C; Pucci F; Liao HW; Lin YJ; Newton A; Yaghi OK; Iwamoto Y; Tricot B; Wojtkiewicz GR; Nahrendorf M; Cortez-Retamozo V; Meylan E; Hynes RO; Demay M; Klein A; Bredella MA; Scadden DT; Weissleder R; Pittet MJ
[Ad] Endereço:Center for Systems Biology, Massachusetts General Hospital Research Institute and Harvard Medical School, Boston, MA 02114, USA.
[Ti] Título:Osteoblasts remotely supply lung tumors with cancer-promoting SiglecF neutrophils.
[So] Source:Science;358(6367), 2017 12 01.
[Is] ISSN:1095-9203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bone marrow-derived myeloid cells can accumulate within tumors and foster cancer outgrowth. Local immune-neoplastic interactions have been intensively investigated, but the contribution of the systemic host environment to tumor growth remains poorly understood. Here, we show in mice and cancer patients ( = 70) that lung adenocarcinomas increase bone stromal activity in the absence of bone metastasis. Animal studies reveal that the cancer-induced bone phenotype involves bone-resident osteocalcin-expressing (Ocn ) osteoblastic cells. These cells promote cancer by remotely supplying a distinct subset of tumor-infiltrating SiglecF neutrophils, which exhibit cancer-promoting properties. Experimentally reducing Ocn cell numbers suppresses the neutrophil response and lung tumor outgrowth. These observations posit osteoblasts as remote regulators of lung cancer and identify SiglecF neutrophils as myeloid cell effectors of the osteoblast-driven protumoral response.
[Mh] Termos MeSH primário: Adenocarcinoma/patologia
Antígenos CD/metabolismo
Antígenos de Diferenciação Mielomonocítica/metabolismo
Osso e Ossos/patologia
Lectinas/metabolismo
Neoplasias Pulmonares/patologia
Infiltração de Neutrófilos
Neutrófilos/metabolismo
Neutrófilos/patologia
Osteoblastos/patologia
[Mh] Termos MeSH secundário: Animais
Densidade Óssea
Células da Medula Óssea/patologia
Osso e Ossos/metabolismo
Linhagem Celular Tumoral
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
Células Mieloides/patologia
Neoplasias Experimentais/patologia
Osteocalcina/metabolismo
Receptor para Produtos Finais de Glicação Avançada/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Antigens, Differentiation, Myelomonocytic); 0 (Lectins); 0 (Receptor for Advanced Glycation End Products); 0 (SIGLEC5 protein, human); 0 (sRAGE protein, human); 104982-03-8 (Osteocalcin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171202
[St] Status:MEDLINE


  4 / 3005 MEDLINE  
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[PMID]:28974473
[Au] Autor:Wang Y; Zhang W; Zhao H; Wang Y; Lu C; Li X; Wang Y; Xiao Y; Wang Y; Wang B
[Ad] Endereço:Department of Physiology, Qiqihar Medical University, Qiqihar, Heilongjiang, PR China.
[Ti] Título:Fasting blood soluble RAGE may be causally implicated in impaired glucose metabolism in Chinese patients with primary hypertension.
[So] Source:Gene;639:11-17, 2018 Jan 10.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:We prepared to investigate the association of four well-defined polymorphisms in the receptor for advanced glycation end-products (RAGE) gene with the changes of fasting blood soluble RAGE (sRAGE) and endogenous secretory RAGE (esRAGE) and the risk for impaired glucose metabolism (IGM) in 1704 patients with primary hypertension, aiming to infer possible causality between sRAGE/esRAGE and IGM. This was a hospital-based case-control study, including 848 patients coexisting with IGM (the case group) and 856 patients with normal glucose tolerance (the control group). Fasting blood sRAGE and esRAGE concentrations were measured in 300 cases and 300 controls. There were significant differences in the genotypes/alleles of T-429C (rs1800625) and T-374A (rs1800624) polymorphisms between the case and control groups after Bonferroni correction (P<0.05/8). Adjusted estimates of above two polymorphisms for IGM risk were remarkably significant, especially under the recessive model (odd ratio [OR], 95% confidence interval [CI], P: 3.57, 1.95-5.18, 0.002 for T-429C and 3.49, 1.42-8.58, 0.007 for T-374A). Mean sRAGE and esRAGE concentrations were significantly higher in controls than in cases (P<0.001). Participants with the rs1800625 -429CC and -429TC genotypes had significantly lower sRAGE (417.3 and 473.6 vs. 502.3pg/mL, P<0.01) and esRAGE (230.1 and 298.0 vs. 340.4pg/mL, P<0.05) concentrations than those with the -429TT genotype in primary hypertensive patients with IGM. Further Mendelian randomization analysis revealed that per 100pg/mL reduction in fasting blood sRAGE and esRAGE was causally associated with 2.40-fold (95% CI: 1.46-3.94) and 2.65-fold (95% CI: 1.24-5.13) increased IGM risk, respectively. Our findings collectively demonstrate that fasting blood sRAGE and esRAGE may be causally implicated in IGM in primary hypertensive patients.
[Mh] Termos MeSH primário: Glicemia/metabolismo
Hipertensão Essencial/metabolismo
Jejum
Receptor para Produtos Finais de Glicação Avançada/sangue
[Mh] Termos MeSH secundário: Idoso
Estudos de Casos e Controles
China
Feminino
Teste de Tolerância a Glucose
Seres Humanos
Masculino
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Receptor for Advanced Glycation End Products)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171227
[Lr] Data última revisão:
171227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171005
[St] Status:MEDLINE


  5 / 3005 MEDLINE  
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[PMID]:28461203
[Au] Autor:Wang Y; Kim HJ; Sparrow JR
[Ad] Endereço:Department of Ophthalmology, Columbia University Medical Center, New York, NY 10032, United States.
[Ti] Título:Quercetin and cyanidin-3-glucoside protect against photooxidation and photodegradation of A2E in retinal pigment epithelial cells.
[So] Source:Exp Eye Res;160:45-55, 2017 07.
[Is] ISSN:1096-0007
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A family of photoreactive retinaldehyde-derived molecules accumulate in retinal pigment epithelial cells with age; this accumulation is implicated in some retinal diseases. One of these compounds is the diretinal fluorophore A2E. Here we compared polyphenols for their ability to suppress the photooxidation and photodegradation of A2E. In cells that had accumulated A2E and were irradiated with short-wavelength light, quercetin, cyanidin-3-glucoside, ferulic acid and chlorogenic acid diminished cellular levels of reactive oxygen species, but only quercetin and cyanidin-3-glucoside promoted cell viability. By chromatographic quantitation, quercetin and cyanidin-3-glucoside reduced the consumption of A2E by photooxidation in both cell- and cell-free assays. With ultra-high performance liquid chromatography-mass spectrometry, quercetin and cyanidin-3-glucoside also inhibited the formation of photooxidized-A2E species. While photodegradation of A2E is known to result in the release of reactive carbonyls, we demonstrated that quercetin and cyanidin-3-glucoside decreased the formation of methylglyoxal adducts in the cells, and reduced the expression of mRNA encoding receptor for advanced glycation end products. These polyphenols also protected glutathione from reaction with photooxidized A2E. In rod outer segments incubated with all-trans-retinal to generate bisretinoid, followed by irradiation, quercetin and cyanidin-3-glucoside reduced release of the lipid peroxidation product 4-hydroxynonenal. In conclusion, quercetin and cyanidin-3-glucoside can guard against photooxidative processes in retina.
[Mh] Termos MeSH primário: Antocianinas/farmacologia
Glucosídeos/farmacologia
Degeneração Macular/prevenção & controle
Fotólise/efeitos dos fármacos
Quercetina/farmacologia
Epitélio Pigmentado da Retina/metabolismo
[Mh] Termos MeSH secundário: Antioxidantes/farmacologia
Células Cultivadas
Cromatografia Líquida de Alta Pressão
Seres Humanos
Degeneração Macular/metabolismo
Degeneração Macular/patologia
Espectrometria de Massas
Aldeído Pirúvico/metabolismo
Receptor para Produtos Finais de Glicação Avançada/metabolismo
Epitélio Pigmentado da Retina/efeitos dos fármacos
Epitélio Pigmentado da Retina/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Anthocyanins); 0 (Antioxidants); 0 (Glucosides); 0 (Receptor for Advanced Glycation End Products); 7084-24-4 (cyanidin 3-O-glucoside); 722KLD7415 (Pyruvaldehyde); 9IKM0I5T1E (Quercetin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171211
[Lr] Data última revisão:
171211
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE


  6 / 3005 MEDLINE  
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[PMID]:28977635
[Au] Autor:Kumar V; Fleming T; Terjung S; Gorzelanny C; Gebhardt C; Agrawal R; Mall MA; Ranzinger J; Zeier M; Madhusudhan T; Ranjan S; Isermann B; Liesz A; Deshpande D; Häring HU; Biswas SK; Reynolds PR; Hammes HP; Peperkok R; Angel P; Herzig S; Nawroth PP
[Ad] Endereço:Department of Medicine I and Clinical Chemistry, University Hospital of Heidelberg, INF 410, Heidelberg, Germany.
[Ti] Título:Homeostatic nuclear RAGE-ATM interaction is essential for efficient DNA repair.
[So] Source:Nucleic Acids Res;45(18):10595-10613, 2017 Oct 13.
[Is] ISSN:1362-4962
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The integrity of genome is a prerequisite for healthy life. Indeed, defects in DNA repair have been associated with several human diseases, including tissue-fibrosis, neurodegeneration and cancer. Despite decades of extensive research, the spatio-mechanical processes of double-strand break (DSB)-repair, especially the auxiliary factor(s) that can stimulate accurate and timely repair, have remained elusive. Here, we report an ATM-kinase dependent, unforeseen function of the nuclear isoform of the Receptor for Advanced Glycation End-products (nRAGE) in DSB-repair. RAGE is phosphorylated at Serine376 and Serine389 by the ATM kinase and is recruited to the site of DNA-DSBs via an early DNA damage response. nRAGE preferentially co-localized with the MRE11 nuclease subunit of the MRN complex and orchestrates its nucleolytic activity to the ATR kinase signaling. This promotes efficient RPA2S4-S8 and CHK1S345 phosphorylation and thereby prevents cellular senescence, IPF and carcinoma formation. Accordingly, loss of RAGE causatively linked to perpetual DSBs signaling, cellular senescence and fibrosis. Importantly, in a mouse model of idiopathic pulmonary fibrosis (RAGE-/-), reconstitution of RAGE efficiently restored DSB-repair and reversed pathological anomalies. Collectively, this study identifies nRAGE as a master regulator of DSB-repair, the absence of which orchestrates persistent DSB signaling to senescence, tissue-fibrosis and oncogenesis.
[Mh] Termos MeSH primário: Proteínas Mutadas de Ataxia Telangiectasia/metabolismo
Reparo do DNA
Receptor para Produtos Finais de Glicação Avançada/metabolismo
[Mh] Termos MeSH secundário: Animais
Núcleo Celular/enzimologia
Núcleo Celular/metabolismo
Senescência Celular
DNA/metabolismo
Quebras de DNA de Cadeia Dupla
Enzimas Reparadoras do DNA/metabolismo
Proteínas de Ligação a DNA/metabolismo
Homeostase
Pulmão/fisiopatologia
Proteína Homóloga a MRE11
Camundongos Endogâmicos C57BL
Camundongos Knockout
Fibrose Pulmonar/genética
Fibrose Pulmonar/fisiopatologia
Receptor para Produtos Finais de Glicação Avançada/genética
Traumatismo por Reperfusão/genética
Traumatismo por Reperfusão/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ager protein, mouse); 0 (DNA-Binding Proteins); 0 (Mre11a protein, mouse); 0 (Receptor for Advanced Glycation End Products); 9007-49-2 (DNA); EC 2.7.1.- (Atr protein, mouse); EC 2.7.11.1 (Ataxia Telangiectasia Mutated Proteins); EC 3.1.- (MRE11 Homologue Protein); EC 6.5.1.- (DNA Repair Enzymes)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171005
[St] Status:MEDLINE
[do] DOI:10.1093/nar/gkx705


  7 / 3005 MEDLINE  
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[PMID]:28926576
[Au] Autor:Caraher EJ; Kwon S; Haider SH; Crowley G; Lee A; Ebrahim M; Zhang L; Chen LC; Gordon T; Liu M; Prezant DJ; Schmidt AM; Nolan A
[Ad] Endereço:Department of Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, New York University School of Medicine, New York, New York, United States of America.
[Ti] Título:Receptor for advanced glycation end-products and World Trade Center particulate induced lung function loss: A case-cohort study and murine model of acute particulate exposure.
[So] Source:PLoS One;12(9):e0184331, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:World Trade Center-particulate matter(WTC-PM) exposure and metabolic-risk are associated with WTC-Lung Injury(WTC-LI). The receptor for advanced glycation end-products (RAGE) is most highly expressed in the lung, mediates metabolic risk, and single-nucleotide polymorphisms at the AGER-locus predict forced expiratory volume(FEV). Our objectives were to test the hypotheses that RAGE is a biomarker of WTC-LI in the FDNY-cohort and that loss of RAGE in a murine model would protect against acute PM-induced lung disease. We know from previous work that early intense exposure at the time of the WTC collapse was most predictive of WTC-LI therefore we utilized a murine model of intense acute PM-exposure to determine if loss of RAGE is protective and to identify signaling/cytokine intermediates. This study builds on a continuing effort to identify serum biomarkers that predict the development of WTC-LI. A case-cohort design was used to analyze a focused cohort of male never-smokers with normal pre-9/11 lung function. Odds of developing WTC-LI increased by 1.2, 1.8 and 1.0 in firefighters with soluble RAGE (sRAGE)≥97pg/mL, CRP≥2.4mg/L, and MMP-9≤397ng/mL, respectively, assessed in a multivariate logistic regression model (ROCAUC of 0.72). Wild type(WT) and RAGE-deficient(Ager-/-) mice were exposed to PM or PBS-control by oropharyngeal aspiration. Lung function, airway hyperreactivity, bronchoalveolar lavage, histology, transcription factors and plasma/BAL cytokines were quantified. WT-PM mice had decreased FEV and compliance, and increased airway resistance and methacholine reactivity after 24-hours. Decreased IFN-γ and increased LPA were observed in WT-PM mice; similar findings have been reported for firefighters who eventually develop WTC-LI. In the murine model, lack of RAGE was protective from loss of lung function and airway hyperreactivity and was associated with modulation of MAP kinases. We conclude that in a multivariate adjusted model increased sRAGE is associated with WTC-LI. In our murine model, absence of RAGE mitigated acute deleterious effects of PM and may be a biologically plausible mediator of PM-related lung disease.
[Mh] Termos MeSH primário: Volume Expiratório Forçado/efeitos dos fármacos
Lesão Pulmonar/etiologia
Lesão Pulmonar/fisiopatologia
Material Particulado/toxicidade
Receptor para Produtos Finais de Glicação Avançada/metabolismo
Ataques Terroristas de 11 de Setembro
[Mh] Termos MeSH secundário: Doença Aguda
Adulto
Animais
Biomarcadores/análise
Biomarcadores/sangue
Hiper-Reatividade Brônquica/etiologia
Líquido da Lavagem Broncoalveolar/química
Estudos de Casos e Controles
Estudos de Coortes
Modelos Animais de Doenças
Feminino
Bombeiros
Seres Humanos
Pulmão/efeitos dos fármacos
Pulmão/patologia
Pulmão/fisiologia
Lesão Pulmonar/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Meia-Idade
Receptor para Produtos Finais de Glicação Avançada/deficiência
Receptor para Produtos Finais de Glicação Avançada/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Particulate Matter); 0 (Receptor for Advanced Glycation End Products)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170920
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184331


  8 / 3005 MEDLINE  
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[PMID]:28887039
[Au] Autor:Kim SJ; Ryu MJ; Han J; Jang Y; Kim J; Lee MJ; Ryu I; Ju X; Oh E; Chung W; Kweon GR; Heo JY
[Ad] Endereço:Department of Biochemistry, Chungnam National University School of Medicine, Daejeon, 301-747, Republic of Korea; Department of Medical Science, Chungnam National University School of Medicine, Daejeon, 301-747, Republic of Korea; Infection Control Convergence Research Center, Chungnam National Univ
[Ti] Título:Activation of the HMGB1-RAGE axis upregulates TH expression in dopaminergic neurons via JNK phosphorylation.
[So] Source:Biochem Biophys Res Commun;493(1):358-364, 2017 Nov 04.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The derangement of tyrosine hydroxylase (TH) activity reduces dopamine synthesis and is implicated in the pathogenesis of Parkinson's disease. However, the extracellular modulator and intracellular regulatory mechanisms of TH have yet to be identified. Recently, high-mobility group box 1 (HMGB1) was reported to be actively secreted from glial cells and is regarded as a mediator of dopaminergic neuronal loss. However, the mechanism for how HMGB1 affects TH expression, particularly through the receptor for advanced glycation endproducts (RAGE), has not yet been investigated. We found that recombinant HMGB1 (rHMGB1) upregulates TH mRNA expression via simultaneous activation of JNK phosphorylation, and this induction of TH expression is blocked by inhibitors of RAGE and JNK. To investigate how TH expression levels change through the HMGB1-RAGE axis as a result of MPP toxicity, we co-treated SN4741 dopaminergic cells with MPP and rHMGB1. rHMGB1 blocked the reduction of TH mRNA following MPP treatment without altering cell survival rates. Our results suggest that HMGB1 upregulates TH expression to maintain dopaminergic neuronal function via activating RAGE, which is dependent on JNK phosphorylation.
[Mh] Termos MeSH primário: Neurônios Dopaminérgicos/fisiologia
Proteína HMGB1/metabolismo
MAP Quinase Quinase 4/metabolismo
Receptor para Produtos Finais de Glicação Avançada/metabolismo
Transdução de Sinais/fisiologia
Tirosina 3-Mono-Oxigenase/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Fosforilação
Ratos
Regulação para Cima/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ager protein, rat); 0 (HMGB1 Protein); 0 (Hbp1 protein, rat); 0 (Receptor for Advanced Glycation End Products); EC 1.14.16.2 (Tyrosine 3-Monooxygenase); EC 2.7.12.2 (MAP Kinase Kinase 4)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170910
[St] Status:MEDLINE


  9 / 3005 MEDLINE  
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[PMID]:28867179
[Au] Autor:Azizan N; Suter MA; Liu Y; Logsdon CD
[Ad] Endereço:Department of Cancer Biology, The University of Texas M.D. Anderson Cancer Center, Houston, TX 77030, USA.
[Ti] Título:RAGE maintains high levels of NFκB and oncogenic Kras activity in pancreatic cancer.
[So] Source:Biochem Biophys Res Commun;493(1):592-597, 2017 Nov 04.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Oncogenic KRas activity is central to several cancer types including pancreatic ductal adenocarcinoma (PDAC) but has been determined to be "undruggable". Recent studies have indicated that oncogenic KRas is not constitutively active but relies on a feed-forward stimulatory mechanism involving NFκB mediated inflammation. In the current study, we investigated the role of the receptor for advanced glycation end-products (RAGE) in maintaining oncogenic signaling in PDAC. We observed that there was a shift in the levels of specific RAGE isoforms and altered cellular localization in PDAC. Furthermore, inhibition of RAGE using a pharmacological antagonist, FPS-ZM1, or a blocking antibody, decreased phosphorylation of IKBα and inhibited Erk activity down-stream of Kras in PDAC cell lines. In vivo, inhibition of RAGE using FPS-ZM1 reduced the growth of PDAC syngeneic orthotopic xenografts and prolonged survival. These data indicate that RAGE plays a central role in maintaining inflammatory signaling in PDAC that benefits tumor growth. These observations support the development of approaches to inhibit the carcinogenic actions of Kras indirectly by blocking the mechanisms which maintain its activity.
[Mh] Termos MeSH primário: Carcinoma Ductal Pancreático/metabolismo
NF-kappa B/metabolismo
Neoplasias Pancreáticas/metabolismo
Proteínas Proto-Oncogênicas p21(ras)/metabolismo
Receptor para Produtos Finais de Glicação Avançada/metabolismo
[Mh] Termos MeSH secundário: Animais
Carcinoma Ductal Pancreático/patologia
Linhagem Celular Tumoral
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
Neoplasias Pancreáticas/patologia
Frações Subcelulares/metabolismo
Frações Subcelulares/patologia
Distribuição Tecidual
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (KRAS protein, human); 0 (NF-kappa B); 0 (Receptor for Advanced Glycation End Products); EC 3.6.5.2 (Kras2 protein, mouse); EC 3.6.5.2 (Proto-Oncogene Proteins p21(ras))
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170905
[St] Status:MEDLINE


  10 / 3005 MEDLINE  
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[PMID]:28821394
[Au] Autor:Lin CH; Cheng YC; Nicol CJ; Lin KH; Yen CH; Chiang MC
[Ad] Endereço:Department of Pediatrics, Taipei City Hospital Zhongxing Branch, Taipei 103, Taiwan.
[Ti] Título:Activation of AMPK is neuroprotective in the oxidative stress by advanced glycosylation end products in human neural stem cells.
[So] Source:Exp Cell Res;359(2):367-373, 2017 Oct 15.
[Is] ISSN:1090-2422
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Advanced glycosylation end products (AGEs) formation is correlated with the pathogenesis of diabetic neuronal damage, but its links with oxidative stress are still not well understood. Metformin, one of the most widely used anti-diabetic drugs, exerts its effects in part by activation of AMP-activated protein kinase (AMPK). Once activated, AMPK regulates many pathways central to metabolism and energy balance including, glucose uptake, glycolysis and fatty acid oxidation. AMPK is also present in neurons, but its role remains unclear. Here, we show that AGE exposure decreases cell viability of human neural stem cells (hNSCs), and that the AMPK agonist metformin reverses this effect, via AMPK-dependent downregulation of RAGE levels. Importantly, hNSCs co-treated with metformin were significantly rescued from AGE-induced oxidative stress, as reflected by the normalization in levels of reactive oxygen species. In addition, compared to AGE-treated hNSCs, metformin co-treatment significantly reversed the activity and mRNA transcript level changes of SOD1/2 and Gpx. Furthermore, hNSCs exposed to AGEs had significantly lower mRNA levels among other components of normal cellular oxidative defenses (GSH, Catalase and HO-1), which were all rescued by co-treatment with metformin. This metformin-mediated protective effect on hNSCs for of both oxidative stress and oxidative defense genes by co-treatment with metformin was blocked by the addition of an AMPK antagonist (Compound C). These findings unveil the protective role of AMPK-dependent metformin signaling during AGE mediated oxidative stress in hNSCs, and suggests patients undergoing AGE-mediated neurodegeneration may benefit from the novel therapeutic use of metformin.
[Mh] Termos MeSH primário: Proteínas Quinases Ativadas por AMP/genética
Produtos Finais de Glicação Avançada/antagonistas & inibidores
Produtos Finais de Glicação Avançada/farmacologia
Hipoglicemiantes/farmacologia
Metformina/farmacologia
Células-Tronco Neurais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Proteínas Quinases Ativadas por AMP/metabolismo
Catalase/genética
Catalase/metabolismo
Proliferação Celular
Células Cultivadas
Ativação Enzimática/efeitos dos fármacos
Regulação da Expressão Gênica
Glutationa/metabolismo
Heme Oxigenase-1/genética
Heme Oxigenase-1/metabolismo
Seres Humanos
Células-Tronco Neurais/citologia
Células-Tronco Neurais/enzimologia
Estresse Oxidativo/efeitos dos fármacos
Espécies Reativas de Oxigênio/antagonistas & inibidores
Espécies Reativas de Oxigênio/metabolismo
Receptor para Produtos Finais de Glicação Avançada/genética
Receptor para Produtos Finais de Glicação Avançada/metabolismo
Transdução de Sinais
Superóxido Dismutase/genética
Superóxido Dismutase/metabolismo
Superóxido Dismutase-1/genética
Superóxido Dismutase-1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AGER protein, human); 0 (Glycation End Products, Advanced); 0 (Hypoglycemic Agents); 0 (Reactive Oxygen Species); 0 (Receptor for Advanced Glycation End Products); 0 (SOD1 protein, human); 9100L32L2N (Metformin); EC 1.11.1.6 (Catalase); EC 1.14.14.18 (HMOX1 protein, human); EC 1.14.14.18 (Heme Oxygenase-1); EC 1.15.1.1 (Superoxide Dismutase); EC 1.15.1.1 (Superoxide Dismutase-1); EC 1.15.1.1 (superoxide dismutase 2); EC 2.7.11.31 (AMP-Activated Protein Kinases); GAN16C9B8O (Glutathione)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170820
[St] Status:MEDLINE



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