Base de dados : MEDLINE
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[PMID]:28467092
[Au] Autor:Wu M; Ye H; Shao C; Zheng X; Li Q; Wang L; Zhao M; Lu G; Chen B; Zhang J; Wang Y; Wang G; Hao H
[Ad] Endereço:Key Laboratory of Drug Metabolism and Pharmacokinetics, State Key Laboratory of Natural Medicines and ‡School of Pharmacy, China Pharmaceutical University , Tongjiaxiang #24, Nanjing 210009, China.
[Ti] Título:Metabolomics-Proteomics Combined Approach Identifies Differential Metabolism-Associated Molecular Events between Senescence and Apoptosis.
[So] Source:J Proteome Res;16(6):2250-2261, 2017 Jun 02.
[Is] ISSN:1535-3907
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Apoptosis and senescence are two types of cell fates in response to chemotherapy. Besides canonical pathways that mediate cell fates, cancer cell metabolism has been revealed as a crucial factor affecting cell fate decisions and thus represents a new target for antitumor therapy. Therefore, a comprehensive description of metabolic pathways underlying cell senescence and apoptosis in response to chemotherapy is highly demanded for therapeutic exploitation of both processes. Herein we employed a metabolomics-proteomics combined approach to identify metabolism-associated molecular events that mediate cellular responses to senescence and apoptosis using doxorubicin-treated human breast cancer cells MCF7 as models. Such biomics approach revealed that tricarboxylic acid cycle, pentose phosphate pathway, and nucleotide synthesis pathways were significantly upregulated in the senescent model, whereas fatty acid synthesis was reduced. In apoptotic cells, an overall reduced activity of major metabolic pathways was observed except for the arginine and proline pathway. Combinatorially, these data show the utility of biomics in exploring biochemical mechanism-based differences between apoptosis and senescence and reveal an unprecedented finding of the metabolic events that were induced for survival by facilitating ROS elimination and DNA damage repair in senescent cells, while they were downregulated in apoptotic cells when DNA damage was irreparable.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Senescência Celular/efeitos dos fármacos
Redes e Vias Metabólicas/efeitos dos fármacos
Metabolômica/métodos
Proteômica/métodos
[Mh] Termos MeSH secundário: Ciclo do Ácido Cítrico
Dano ao DNA
Doxorrubicina/farmacologia
Doxorrubicina/uso terapêutico
Ácidos Graxos/biossíntese
Seres Humanos
Células MCF-7
Nucleotídeos/biossíntese
Via de Pentose Fosfato
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fatty Acids); 0 (Nucleotides); 0 (Reactive Oxygen Species); 80168379AG (Doxorubicin)
[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:170504
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jproteome.7b00111


  2 / 13680 MEDLINE  
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[PMID]:29412148
[Au] Autor:Hou J; Cui C; Kim S; Sung C; Choi C
[Ad] Endereço:Intelligent Synthetic Biology Center, Daejeon 34141, Republic of Korea.
[Ti] Título:Ginsenoside F1 suppresses astrocytic senescence-associated secretory phenotype.
[So] Source:Chem Biol Interact;283:75-83, 2018 Mar 01.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Senescence is one of the hallmarks of aging and identified as a potential therapeutic target in the treatment of aging and aging-related diseases. Senescent cells accumulate with age in a variety of human tissues where they develop a complex senescence-associated secretory phenotype (SASP). SASP in brain could contribute to age-related inflammation and chronic neurodegenerative diseases. We confirmed that senescent astrocytes express a characteristic of SASP in vitro by human cytokine antibody array. Ginsenoside F1 suppresses the SASP from astrocytes induced by d-galactose via suppressing p38MAPK-dependent NF-κB activity. A specific inhibitor of p38MAPK, SB203580 significantly decreased the secretion of IL-6 and IL-8, the major components of SASPs. Additionally, treatment of senescent astrocytes with NF-κB inhibitor, BAY 11-7092, also suppressed the secretion of IL-6 and IL-8, suggesting NF-κB was required for SASP. Importantly, conditioned media from senescent astrocytes promoted the migration of glioblastoma cells, such as U373-MG, U251-MG and U87-MG assessed by scratch wound healing. This migration was significantly decreased by F1 treatment in senescent astrocytes. Interestingly, IL-8, the main mediator regulating glioblastoma cell invasion, was suppressed in both transcriptional and protein level. Herein, we propose ginsenoside F1 as a potential therapeutic strategy for reducing the deleterious contribution of senescent astrocytes in aged brain and related diseases.
[Mh] Termos MeSH primário: Senescência Celular/efeitos dos fármacos
Ginsenosídeos/farmacologia
[Mh] Termos MeSH secundário: Astrócitos/citologia
Astrócitos/efeitos dos fármacos
Astrócitos/metabolismo
Linhagem Celular
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Reparo do DNA/efeitos dos fármacos
Ensaio de Imunoadsorção Enzimática
Seres Humanos
Imidazóis/farmacologia
Interleucina-6/análise
Interleucina-6/metabolismo
Interleucina-8/análise
Interleucina-8/metabolismo
NF-kappa B/antagonistas & inibidores
NF-kappa B/metabolismo
Fosforilação/efeitos dos fármacos
Piridinas/farmacologia
Transdução de Sinais/efeitos dos fármacos
Proteínas Quinases p38 Ativadas por Mitógeno/antagonistas & inibidores
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ginsenosides); 0 (Imidazoles); 0 (Interleukin-6); 0 (Interleukin-8); 0 (NF-kappa B); 0 (Pyridines); 53963-43-2 (ginsenoside F1); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases); OU13V1EYWQ (SB 203580)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180208
[St] Status:MEDLINE


  3 / 13680 MEDLINE  
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[PMID]:29339767
[Au] Autor:Liu X; Mo W; Ye J; Li L; Zhang Y; Hsueh EC; Hoft DF; Peng G
[Ad] Endereço:Department of Internal Medicine, Division of Infectious Diseases, Allergy & Immunology, Saint Louis University School of Medicine, St Louis, MO, 63104, USA.
[Ti] Título:Regulatory T cells trigger effector T cell DNA damage and senescence caused by metabolic competition.
[So] Source:Nat Commun;9(1):249, 2018 01 16.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Defining the suppressive mechanisms used by regulatory T (Treg) cells is critical for the development of effective strategies for treating tumors and chronic infections. The molecular processes that occur in responder T cells that are suppressed by Treg cells are unclear. Here we show that human Treg cells initiate DNA damage in effector T cells caused by metabolic competition during cross-talk, resulting in senescence and functional changes that are molecularly distinct from anergy and exhaustion. ERK1/2 and p38 signaling cooperate with STAT1 and STAT3 to control Treg-induced effector T-cell senescence. Human Treg-induced T-cell senescence can be prevented via inhibition of the DNA damage response and/or STAT signaling in T-cell adoptive transfer mouse models. These studies identify molecular mechanisms of human Treg cell suppression and indicate that targeting Treg-induced T-cell senescence is a checkpoint for immunotherapy against cancer and other diseases associated with Treg cells.
[Mh] Termos MeSH primário: Dano ao DNA
Sistema de Sinalização das MAP Quinases
Linfócitos T Reguladores/fisiologia
[Mh] Termos MeSH secundário: Senescência Celular
Glucose/metabolismo
Seres Humanos
Imunoterapia
Fator de Transcrição STAT1/metabolismo
Fator de Transcrição STAT1/fisiologia
Fator de Transcrição STAT3/metabolismo
Fator de Transcrição STAT3/fisiologia
Linfócitos T Reguladores/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 (STAT1 Transcription Factor); 0 (STAT1 protein, human); 0 (STAT3 Transcription Factor); 0 (STAT3 protein, human); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180118
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02689-5


  4 / 13680 MEDLINE  
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[PMID]:29311544
[Au] Autor:Bernardes de Jesus B; Marinho SP; Barros S; Sousa-Franco A; Alves-Vale C; Carvalho T; Carmo-Fonseca M
[Ad] Endereço:Instituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, 1649-028, Lisboa, Portugal. bruno.jesus@medicina.ulisboa.pt.
[Ti] Título:Silencing of the lncRNA Zeb2-NAT facilitates reprogramming of aged fibroblasts and safeguards stem cell pluripotency.
[So] Source:Nat Commun;9(1):94, 2018 01 08.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Aging imposes a barrier to somatic cell reprogramming through poorly understood mechanisms. Here, we report that fibroblasts from old mice express higher levels of Zeb2, a transcription factor that activates epithelial-to-mesenchymal transition. Synthesis of Zeb2 protein is controlled by a natural antisense transcript named Zeb2-NAT. We show that transfection of adult fibroblasts with specific LNA Gapmers induces a robust downregulation of Zeb2-NAT transcripts and Zeb2 protein and enhances the reprogramming of old fibroblasts into pluripotent cells. We further demonstrate that Zeb2-NAT expression is precociously activated by differentiation stimuli in embryonic stem (ES) cells. By knocking down Zeb2-NAT, we were able to maintain ES cells challenged with commitment signals in the ground state of pluripotency. In conclusion, our study identifies a long noncoding RNA that is overlapping and antisense to the Zeb2 locus as a target for rejuvenation strategies.
[Mh] Termos MeSH primário: Reprogramação Celular/genética
Senescência Celular/genética
Fibroblastos/citologia
RNA Longo não Codificante/fisiologia
Homeobox 2 de Ligação a E-box com Dedos de Zinco/metabolismo
[Mh] Termos MeSH secundário: Animais
Fibroblastos/metabolismo
Regulação da Expressão Gênica
Técnicas de Silenciamento de Genes
Inativação Gênica
Camundongos
Células-Tronco Pluripotentes
RNA Antissenso/fisiologia
Homeobox 2 de Ligação a E-box com Dedos de Zinco/genética
Homeobox 2 de Ligação a E-box com Dedos de Zinco/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (RNA, Antisense); 0 (RNA, Long Noncoding); 0 (ZEB2 protein, mouse); 0 (Zinc Finger E-box Binding Homeobox 2)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180110
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-01921-6


  5 / 13680 MEDLINE  
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[PMID]:28460440
[Au] Autor:Massari NA; Nicoud MB; Sambuco L; Cricco GP; Martinel Lamas DJ; Herrero Ducloux MV; Blanco H; Rivera ES; Medina VA
[Ad] Endereço:Laboratory of Radioisotopes, School of Pharmacy and Biochemistry, University of Buenos Aires, Buenos Aires, Argentina.
[Ti] Título:Histamine therapeutic efficacy in metastatic melanoma: Role of histamine H4 receptor agonists and opportunity for combination with radiation.
[So] Source:Oncotarget;8(16):26471-26491, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The aims of the work were to improve our knowledge of the role of H4R in melanoma proliferation and assess in vivo the therapeutic efficacy of histamine, clozapine and JNJ28610244, an H4R agonist, in a preclinical metastatic model of melanoma. Additionally, we aimed to investigate the combinatorial effect of histamine and gamma radiation on the radiobiological response of melanoma cells.Results indicate that 1205Lu metastatic melanoma cells express H4R and that histamine inhibits proliferation, in part through the stimulation of the H4R, and induces cell senescence and melanogenesis. Daily treatment with H4R agonists (1 mg/kg, sc) exhibited a significant in vivo antitumor effect and importantly, compounds reduced metastatic potential, particularly in the group treated with JNJ28610244, the H4R agonist with higher specificity. H4R is expressed in benign and malignant lesions of melanocytic lineage, highlighting the potential clinical use of histamine and H4R agonists. In addition, histamine increased radiosensitivity of melanoma cells in vitro and in vivo. We conclude that stimulation of H4R by specific ligands may represent a novel therapeutic strategy in those tumors that express this receptor. Furthermore, through increasing radiation-induced response, histamine could improve cancer radiotherapy for the treatment of melanoma.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Histamina/farmacologia
Melanoma/metabolismo
Melanoma/patologia
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/uso terapêutico
Biomarcadores
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Senescência Celular/efeitos dos fármacos
Terapia Combinada
Modelos Animais de Doenças
Histamina/uso terapêutico
Seres Humanos
Imuno-Histoquímica
Indóis/farmacologia
Melanoma/terapia
Camundongos
Camundongos Nus
Metástase Neoplásica
Estadiamento de Neoplasias
Oximas/farmacologia
Radiação Ionizante
Receptores Histamínicos H4/metabolismo
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Biomarkers); 0 (Indoles); 0 (JNJ28610244); 0 (Oximes); 0 (Receptors, Histamine H4); 820484N8I3 (Histamine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15594


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[PMID]:28468668
[Au] Autor:Flowers A; Bell-Temin H; Jalloh A; Stevens SM; Bickford PC
[Ad] Endereço:Department of Neurosurgery and Brain Repair, USF Health Morsani College of Medicine, University of South Florida, 12901 Bruce B Downs Blvd., Campus Box MDC-78, Tampa, FL, 33570, USA.
[Ti] Título:Proteomic anaysis of aged microglia: shifts in transcription, bioenergetics, and nutrient response.
[So] Source:J Neuroinflammation;14(1):96, 2017 May 03.
[Is] ISSN:1742-2094
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Age is the primary risk factor for many diseases. As such, age is a critical co-factor for examination in order to understand the progression and potential intervention in disease progression. Studies examining both the phenotype and transcriptome of aged microglia demonstrated a propensity for the development of a pro-inflammatory phenotype. Less well studied is the concomitant blunting of anti-inflammatory aspects of microglial function with age which also impact plasticity and repair in the CNS. METHODS: This study utilizes mass spectrometry-based proteomics to compare primary microglia from young and aged animals. RESULTS: This study revealed alterations in three clusters of inter-related proteins. The three pathways were inflammatory signaling, mitochondrial function, and cellular metabolism. Analysis of these clusters identified the protein rapamycin-insensitive companion of mTOR (RICTOR), a component of the mTORC2 complex, as a novel upstream regulator of several biological functions that are altered with age and potentially linked to phenotype development. A decrease in mTORC2-dependent AKT S473 phosphorylation, as assessed by insulin growth factor (IGF) treatment, was observed in aged microglia. This novel finding was confirmed by genetic manipulation of the microglial cell line. BV2 cells with diminished RICTOR displayed a phenotype that was strikingly similar to that of aged microglia. This finding is particularly relevant as the mTOR pathway already has a number of pharmacological modulators used clinically. CONCLUSIONS: The results suggest that microglia from aged mice show changes in cellular metabolism and energy regulation that might underlie the alterations in inflammatory signaling. Modulation of one pathway identified in our bioinformatic analysis, RICTOR, may provide an avenue by which deleterious aspects of the aging microglia can be attenuated. If successful, this could mean potentially delaying or diminishing the progress of diseases for which progressive inflammation is involved.
[Mh] Termos MeSH primário: Senescência Celular/fisiologia
Metabolismo Energético/fisiologia
Microglia/metabolismo
Mapas de Interação de Proteínas/fisiologia
Proteômica/métodos
Transcrição Genética/fisiologia
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Ácidos Graxos/metabolismo
Alimentos
Glucose/metabolismo
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fatty Acids); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1186/s12974-017-0840-7


  7 / 13680 MEDLINE  
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[PMID]:28743715
[Au] Autor:Tak T; Drylewicz J; Conemans L; de Boer RJ; Koenderman L; Borghans JAM; Tesselaar K
[Ad] Endereço:Department of Respiratory Medicine and.
[Ti] Título:Circulatory and maturation kinetics of human monocyte subsets in vivo.
[So] Source:Blood;130(12):1474-1477, 2017 09 21.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Monócitos/citologia
[Mh] Termos MeSH secundário: Asma/sangue
Diferenciação Celular
Senescência Celular
Replicação do DNA
Eosinofilia/sangue
Feminino
Proteínas Ligadas por GPI/análise
Homeostase
Seres Humanos
Imunofenotipagem
Cinética
Contagem de Leucócitos
Receptores de Lipopolissacarídeos/análise
Masculino
Modelos Biológicos
Monócitos/química
Monócitos/classificação
Receptores de IgG/análise
Valores de Referência
[Pt] Tipo de publicação:LETTER; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (FCGR3B protein, human); 0 (GPI-Linked Proteins); 0 (Lipopolysaccharide Receptors); 0 (Receptors, IgG)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2017-03-771261


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[PMID]:28448963
[Au] Autor:Rinaldi S; Pallikkuth S; George VK; de Armas LR; Pahwa R; Sanchez CM; Pallin MF; Pan L; Cotugno N; Dickinson G; Rodriguez A; Fischl M; Alcaide M; Gonzalez L; Palma P; Pahwa S
[Ad] Endereço:Miami Center for AIDS Research, Department of Microbiology and Immunology, University of Miami Miller School of Medicine, Miami, FL 33136, USA.
[Ti] Título:Paradoxical aging in HIV: immune senescence of B Cells is most prominent in young age.
[So] Source:Aging (Albany NY);9(4):1307-1325, 2017 Apr.
[Is] ISSN:1945-4589
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Combination antiretroviral therapies (cART)can lead to normal life expectancy in HIV-infected persons, and people aged >50 yrs represent the fastest growing HIV group. Although HIV and aging are independently associated with impaired humoral immunity, immune status in people aging with HIV is relatively unexplored. In this study influenza vaccination was used to probe age associated perturbations in the B cell compartment of HIV-negative "healthy controls" (HC) and virologically controlled HIV-infected participants on cART (HIV) (n=124), grouped by age as young (<40 yrs), middle-aged (40-59yrs) or old ( 60 yrs). H1N1 antibody response at d21 post-vaccination correlated inversely with age in both HC and HIV. Immunophenotyping of cryopreserved PBMC demonstrated increased frequencies of double negative B cells and decreased plasmablasts in old compared to young HC. Remarkably, young HIV were different from young HC but similar to old HC in B cell phenotype, influenza specific spontaneous (d7) or memory (d21) antibody secreting cells. We conclude that B cell immune senescence is a prominent phenomenon in young HIV in comparison to young HC, but distinctions between old HIV and old HC are less evident though both groups manifest age-associated B cell dysfunction.
[Mh] Termos MeSH primário: Linfócitos B/imunologia
Senescência Celular/imunologia
Infecções por HIV/imunologia
Infecções por HIV/patologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Envelhecimento/imunologia
Envelhecimento/patologia
Anticorpos Antivirais/biossíntese
Feminino
Testes de Inibição da Hemaglutinação
Seres Humanos
Memória Imunológica
Vírus da Influenza A Subtipo H1N1/imunologia
Vacinas contra Influenza
Masculino
Meia-Idade
Vacinação
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Viral); 0 (Influenza Vaccines)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE
[do] DOI:10.18632/aging.101229


  9 / 13680 MEDLINE  
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[PMID]:29315311
[Au] Autor:Hwang HV; Tran DT; Rebuffatti MN; Li CS; Knowlton AA
[Ad] Endereço:Molecular & Cellular Cardiology, Cardiovascular Division, Department of Internal Medicine, University of California-Davis, Davis, CA, United States of America.
[Ti] Título:Investigation of quercetin and hyperoside as senolytics in adult human endothelial cells.
[So] Source:PLoS One;13(1):e0190374, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:NEW AND NOTEWORTHY: Previously, quercetin has been reported to be a senolytic, a drug that selectively removes senescent cells, in HUVECs. However, we found neither quercetin nor Q3G was effective as a senolytic for adult human endothelial cells.
[Mh] Termos MeSH primário: Senescência Celular/efeitos dos fármacos
Endotélio Vascular/efeitos dos fármacos
Quercetina/análogos & derivados
Quercetina/farmacologia
[Mh] Termos MeSH secundário: Adulto
Proliferação Celular/efeitos dos fármacos
Endotélio Vascular/citologia
Feminino
Células Endoteliais da Veia Umbilical Humana
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
8O1CR18L82 (hyperoside); 9IKM0I5T1E (Quercetin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180110
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190374


  10 / 13680 MEDLINE  
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[PMID]:29190775
[Au] Autor:Ahn SH; Chun S; Park C; Lee JH; Lee SW; Lee TH
[Ad] Endereço:Department of Oral Biochemistry, Dental Science Research Institute, Medical Research Center for Biomineralization Disorders, School of Dentistry, Chonnam National University, Gwangju, Republic of Korea.
[Ti] Título:Transcriptome profiling analysis of senescent gingival fibroblasts in response to Fusobacterium nucleatum infection.
[So] Source:PLoS One;12(11):e0188755, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Periodontal disease is caused by dental plaque biofilms. Fusobacterium nucleatum is an important periodontal pathogen involved in the development of bacterial complexity in dental plaque biofilms. Human gingival fibroblasts (GFs) act as the first line of defense against oral microorganisms and locally orchestrate immune responses by triggering the production of reactive oxygen species and pro-inflammatory cytokines (IL-6 and IL-8). The frequency and severity of periodontal diseases is known to increase in elderly subjects. However, despite several studies exploring the effects of aging in periodontal disease, the underlying mechanisms through which aging affects the interaction between F. nucleatum and human GFs remain unclear. To identify genes affected by infection, aging, or both, we performed an RNA-Seq analysis using GFs isolated from a single healthy donor that were passaged for a short period of time (P4) 'young GFs' or for longer period of time (P22) 'old GFs', and infected or not with F. nucleatum. Comparing F. nucleatum-infected and uninfected GF(P4) cells the differentially expressed genes (DEGs) were involved in host defense mechanisms (i.e., immune responses and defense responses), whereas comparing F. nucleatum-infected and uninfected GF(P22) cells the DEGs were involved in cell maintenance (i.e., TGF-ß signaling, skeletal development). Most DEGs in F. nucleatum-infected GF(P22) cells were downregulated (85%) and were significantly associated with host defense responses such as inflammatory responses, when compared to the DEGs in F. nucleatum-infected GF(P4) cells. Five genes (GADD45b, KLF10, CSRNP1, ID1, and TM4SF1) were upregulated in response to F. nucleatum infection; however, this effect was only seen in GF(P22) cells. The genes identified here appear to interact with each other in a network associated with free radical scavenging, cell cycle, and cancer; therefore, they could be potential candidates involved in the aged GF's response to F. nucleatum infection. Further studies are needed to confirm these observations.
[Mh] Termos MeSH primário: Fusobacterium nucleatum/patogenicidade
Perfilação da Expressão Gênica
Gengiva/metabolismo
Transcriptoma
[Mh] Termos MeSH secundário: Células Cultivadas
Senescência Celular
Fibroblastos/metabolismo
Fibroblastos/microbiologia
Gengiva/citologia
Gengiva/microbiologia
Seres Humanos
Análise de Sequência de RNA
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188755



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