Base de dados : MEDLINE
Pesquisa : D23.035 [Categoria DeCS]
Referências encontradas : 96 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 10 ir para página                        

  1 / 96 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29386427
[Au] Autor:Tachibana M
[Ad] Endereço:Laboratory of Biotechnology and Therapeutics, Graduate School of Pharmaceutical Sciences, Osaka University.
[Ti] Título:[The Immunosuppressive Function of Myeloid-derived Suppressor Cells Is Regulated by the HMGB1-TLR4 Axis].
[So] Source:Yakugaku Zasshi;138(2):143-148, 2018.
[Is] ISSN:1347-5231
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo: Myeloid-derived suppressor cells (MDSCs) accumulate under pathological conditions, including cancer and chronic inflammation, and they suppress various immune responses such as T cell proliferation. Although several inflammatory signals enhance the differentiation and/or function of MDSCs, it is not clear which factors regulate their differentiation and immunosuppressive function. It has been highlighted that damage-associated molecular patterns (DAMPs) play important roles in the induction of inflammation. One of the DAMPs, the high mobility group box 1 (HMGB1), is released from necrotic cells and secreted by macrophages. It has been shown that HMGB1 level is elevated in tumors and tumor-bearing hosts. It has also been reported that HMGB1 transduces intracellular signaling via several receptors, including the receptor for advanced glycation end-products (RAGE) and the toll-like receptor (TLR)4, both of which enhance the differentiation and/or function of MDSCs. However, the effects of HMGB1 on MDSCs remain unclear. In the present study, we examined the effect of HMGB1 on in vitro MDSC differentiation and immunosuppressive functions. Since murine bone marrow (BM) cells can differentiate into MDSCs upon granulocyte-macrophage colony-stimulating factor (GM-CSF) stimulation for 4 d in vitro, we cultured murine BM cells in the presence of HMGB1 and GM-CSF. The results demonstrated that HMGB1 enhanced the suppressive activity of in vitro MDSCs, depending on TLR4, whereas lipopolysaccharide (LPS), one of the TLR4 ligands, interfered with this differentiation and immunosuppressive activity of in vitro MDSCs, depending on TLR4. Our findings thus suggest that the HMGB1-TLR4 axis enhances the immunosuppressive function of MDSCs.
[Mh] Termos MeSH primário: Células da Medula Óssea/imunologia
Proteína HMGB1/fisiologia
Imunossupressão
Transdução de Sinais/fisiologia
Receptor 4 Toll-Like/fisiologia
[Mh] Termos MeSH secundário: Alarminas
Animais
Células da Medula Óssea/citologia
Diferenciação Celular
Produtos Finais de Glicação Avançada
Seres Humanos
Inflamação/imunologia
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Alarmins); 0 (Glycation End Products, Advanced); 0 (HMGB1 Protein); 0 (Toll-Like Receptor 4)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180202
[St] Status:MEDLINE
[do] DOI:10.1248/yakushi.17-00158


  2 / 96 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28746820
[Au] Autor:Rai V; Agrawal DK
[Ad] Endereço:Department of Clinical and Translational Science, Creighton University School of Medicine, Omaha, NE 68178, USA.
[Ti] Título:The role of damage- and pathogen-associated molecular patterns in inflammation-mediated vulnerability of atherosclerotic plaques.
[So] Source:Can J Physiol Pharmacol;95(10):1245-1253, 2017 Oct.
[Is] ISSN:1205-7541
[Cp] País de publicação:Canada
[La] Idioma:eng
[Ab] Resumo:Atherosclerosis is a chronic inflammatory disease resulting in the formation of the atherosclerotic plaque. Plaque formation starts with the inflammation in fatty streaks and progresses through atheroma, atheromatous plaque, and fibroatheroma leading to development of stable plaque. Hypercholesterolemia, dyslipidemia, and hyperglycemia are the risk factors for atherosclerosis. Inflammation, infection with viruses and bacteria, and dysregulation in the endothelial and vascular smooth muscle cells leads to advanced plaque formation. Death of the cells in the intima due to inflammation results in secretion of damage-associated molecular patterns (DAMPs) such as high mobility group box 1 (HMGB1), receptor for advanced glycation end products (RAGE), alarmins (S100A8, S100A9, S100A12, and oxidized low-density lipoproteins), and infection with pathogens leads to secretion of pathogen-associated molecular patterns (PAMPs) such as lipopolysaccharides, lipoteichoic acids, and peptidoglycans. DAMPs and PAMPs further activate the inflammatory surface receptors such as TREM-1 and toll-like receptors and downstream signaling kinases and transcription factors leading to increased secretion of pro-inflammatory cytokines such as tumor necrosis factor α, interleukin (IL)-1ß, IL-6, and interferon-γ and matrix metalloproteinases (MMPs). These mediators and cytokines along with MMPs render the plaque vulnerable for rupture leading to ischemic events. In this review, we have discussed the role of DAMPs and PAMPs in association with inflammation-mediated plaque vulnerability.
[Mh] Termos MeSH primário: Alarminas/metabolismo
Artérias/metabolismo
Aterosclerose/metabolismo
Mediadores da Inflamação/metabolismo
Inflamação/metabolismo
Padrões Moleculares Associados a Patógenos/metabolismo
Placa Aterosclerótica
[Mh] Termos MeSH secundário: Alarminas/imunologia
Animais
Artérias/imunologia
Artérias/patologia
Aterosclerose/imunologia
Aterosclerose/patologia
Seres Humanos
Inflamação/imunologia
Inflamação/patologia
Mediadores da Inflamação/imunologia
Padrões Moleculares Associados a Patógenos/imunologia
Prognóstico
Fatores de Risco
Ruptura Espontânea
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Alarmins); 0 (Inflammation Mediators); 0 (Pathogen-Associated Molecular Pattern Molecules)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180205
[Lr] Data última revisão:
180205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.1139/cjpp-2016-0664


  3 / 96 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28452964
[Au] Autor:Picca A; Lezza AMS; Leeuwenburgh C; Pesce V; Calvani R; Landi F; Bernabei R; Marzetti E
[Ad] Endereço:Department of Geriatrics, Neuroscience and Orthopedics, Catholic University of the Sacred Heart School of Medicine, 00168 Rome, Italy. anna.picca1@gmail.com.
[Ti] Título:Fueling Inflamm-Aging through Mitochondrial Dysfunction: Mechanisms and Molecular Targets.
[So] Source:Int J Mol Sci;18(5), 2017 Apr 28.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Among the complex determinants of aging, mitochondrial dysfunction has been in the spotlight for a long time. As the hub for many cellular functions, the maintenance of an adequate pool of functional mitochondria is crucial for tissue homeostasis. Their unique role in energy supply makes these organelles essential, especially in those tissues strictly dependent on oxidative metabolism. Mitochondrial quality control (MQC) is ensured by pathways related to protein folding and degradation as well as by processes involving the entire organelle, such as biogenesis, dynamics, and mitophagy. Dysfunctional MQC, oxidative stress and inflammation are hallmarks of senescence and chronic degenerative diseases. One of the consequences of age-related failing MQC and oxidative stress is the release of mitochondria-derived damage-associated molecular patterns (DAMPs). Through their bacterial ancestry, these molecules contribute to mounting an inflammatory response by interacting with receptors similar to those involved in pathogen-associated responses. Mitochondrial DAMPs, especially cell-free mitochondrial DNA, have recently become the subject of intensive research because of their possible involvement in conditions associated with inflammation, such as aging and degenerative diseases. Here, we review the contribution of mitochondrial DAMPs to inflammation and discuss some of the mechanisms at the basis of their generation.
[Mh] Termos MeSH primário: Envelhecimento
Inflamação
Mitocôndrias/metabolismo
[Mh] Termos MeSH secundário: Alarminas/metabolismo
DNA Mitocondrial/metabolismo
Seres Humanos
Mitocôndrias/genética
Degradação Mitocondrial
Dinâmica Mitocondrial
Estresse Oxidativo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Alarmins); 0 (DNA, Mitochondrial)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180122
[Lr] Data última revisão:
180122
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE


  4 / 96 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29193305
[Au] Autor:Blom K; Elshafie AI; Jönsson UB; Rönnelid J; Håkansson LD; Venge P
[Ad] Endereço:Department of Medical Sciences, Clinical Chemistry, Uppsala University, Uppsala, Sweden.
[Ti] Título:The genetically determined production of the alarmin eosinophil-derived neurotoxin is reduced in visceral leishmaniasis.
[So] Source:APMIS;126(1):85-91, 2018 Jan.
[Is] ISSN:1600-0463
[Cp] País de publicação:Denmark
[La] Idioma:eng
[Ab] Resumo:Visceral leishmaniasis (VL) is the most severe form of leishmaniasis. Recent findings indicate that dendritic cells have a key role in the defense against the Leishmania parasite and that the activity of this cell may be modified by the eosinophil secretory protein eosinophil-derived neurotoxin (EDN). We hypothesized that the interactions between dendritic cells and EDN might be of importance in the disease development. Cellular content of EDN was analyzed by ELISA. The single-nucleotide polymorphisms at positions 405, 416, and 1122 in the EDN gene were analyzed by real-time PCR with TaqMan reagents. The study cohorts comprised 239 Sudanese subjects (65 healthy controls and 174 with VL) and 300 healthy Swedish controls. The eosinophil content of EDN was lower in VL as compared with controls (p < 0.0001). The EDN405 (G>C) genotype distribution was similar among Swedish and Sudanese controls, whereas VL subjects had a higher prevalence of the EDN405-GG genotype (p < 0.0001). The content of EDN in the eosinophils was closely linked to the EDN405 polymorphism (p = 0.0002). Our findings suggest that the predisposition to acquire VL is related to the genetic polymorphism of the EDN gene and the reduced production by the eosinophil of this gene product.
[Mh] Termos MeSH primário: Alarminas/genética
Neurotoxina Derivada de Eosinófilo/genética
Leishmaniose Visceral/genética
[Mh] Termos MeSH secundário: Células Dendríticas/imunologia
Predisposição Genética para Doença
Genótipo
Seres Humanos
Leishmaniose Visceral/imunologia
Polimorfismo de Nucleotídeo Único
Receptor 2 Toll-Like/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Alarmins); 0 (TLR2 protein, human); 0 (Toll-Like Receptor 2); EC 3.1.- (Eosinophil-Derived Neurotoxin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171202
[St] Status:MEDLINE
[do] DOI:10.1111/apm.12780


  5 / 96 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28911261
[Au] Autor:Klee NS; McCarthy CG; Martinez-Quinones P; Webb RC
[Ad] Endereço:Department of Physiology, Medical College of Georgia at Augusta University, 1120 15th Street, Augusta, GA 30912, USA.
[Ti] Título:Out of the frying pan and into the fire: damage-associated molecular patterns and cardiovascular toxicity following cancer therapy.
[So] Source:Ther Adv Cardiovasc Dis;11(11):297-317, 2017 Nov.
[Is] ISSN:1753-9455
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cardio-oncology is a new and rapidly expanding field that merges cancer and cardiovascular disease. Cardiovascular disease is an omnipresent side effect of cancer therapy; in fact, it is the second leading cause of death in cancer survivors after recurrent cancer. It has been well documented that many cancer chemotherapeutic agents cause cardiovascular toxicity. Nonetheless, the underlying cause of cancer therapy-induced cardiovascular toxicity is largely unknown. In this review, we discuss the potential role of damage-associated molecular patterns (DAMPs) as an underlying contributor to cancer therapy-induced cardiovascular toxicity. With an increasing number of cancer patients, as well as extended life expectancy, understanding the mechanisms underlying cancer therapy-induced cardiovascular disease is of the utmost importance to ensure that cancer is the only disease burden that cancer survivors have to endure.
[Mh] Termos MeSH primário: Alarminas/metabolismo
Antineoplásicos/efeitos adversos
Doenças Cardiovasculares/induzido quimicamente
Sistema Cardiovascular/efeitos dos fármacos
Sistema Cardiovascular/efeitos da radiação
Neoplasias/terapia
Lesões por Radiação/etiologia
[Mh] Termos MeSH secundário: Animais
Cardiotoxicidade
Doenças Cardiovasculares/metabolismo
Doenças Cardiovasculares/patologia
Doenças Cardiovasculares/fisiopatologia
Sistema Cardiovascular/metabolismo
Sistema Cardiovascular/patologia
Morte Celular/efeitos dos fármacos
Morte Celular/efeitos da radiação
Seres Humanos
Lesões por Radiação/metabolismo
Lesões por Radiação/patologia
Lesões por Radiação/fisiopatologia
Radioterapia/efeitos adversos
Medição de Risco
Fatores de Risco
Transdução de Sinais/efeitos dos fármacos
Transdução de Sinais/efeitos da radiação
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Alarmins); 0 (Antineoplastic Agents)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170916
[St] Status:MEDLINE
[do] DOI:10.1177/1753944717729141


  6 / 96 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28608409
[Au] Autor:Murakami T; Homma Y; Matsuyama R; Mori R; Miyake K; Tanaka Y; Den K; Nagashima Y; Nakazawa M; Hiroshima Y; Ueda M; Tanaka K; Hoffman RM; Bouvet M; Endo I
[Ad] Endereço:Department of Gastroenterological Surgery, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
[Ti] Título:Neoadjuvant chemoradiotherapy of pancreatic cancer induces a favorable immunogenic tumor microenvironment associated with increased major histocompatibility complex class I-related chain A/B expression.
[So] Source:J Surg Oncol;116(3):416-426, 2017 Sep.
[Is] ISSN:1096-9098
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Damage-associated molecular patterns (DAMPs) are related to immune responses in malignant tumors including tumor-infiltrating lymphocytes (TILs). The aim of the present study was to determine the relationship between expression of components of DAMPs and TILs in pancreatic cancer patients who underwent neoadjuvant chemoradiotherapy (NACRT) versus those who did not. METHODS: NACRT was administered to 51 patients with borderline-resectable pancreatic cancer and not to 33 patients with resectable pancreatic cancer. Resected specimens were analyzed for the presence of DAMPs, major histocompatibility complex class I-related chain A/B (MICA/B), and CD8 TILs, CD4 TILs, and forkhead box P3 positive (Foxp3 ) TILs. The Treg/TIL ratio was obtained by dividing the number of Foxp3 TILs, a surrogate for regulatory T cells, by the sum of CD8 and CD4 TILs. RESULTS: Overexpression of calreticulin, Hsp70, and MICA/B were all significantly correlated with NACRT administration. In the NACRT group, high MICA/B expression was associated with a low Treg/TIL ratio, indicating a favorable immunogenic tumor microenvironment. Patients with a lower Treg/TIL ratio had longer survival. CONCLUSIONS: Overexpression of MICA/B, a component of DAMPs induced by NACRT, may play an important role in acquiring a favorable immune response for pancreatic cancer which contributes to longer survival, suggesting the potential of immunotherapy of this recalcitrant disease, especially for patients with overexpression of DAMPs.
[Mh] Termos MeSH primário: Quimiorradioterapia
Antígenos de Histocompatibilidade Classe I/metabolismo
Terapia Neoadjuvante
Neoplasias Pancreáticas/metabolismo
Neoplasias Pancreáticas/terapia
[Mh] Termos MeSH secundário: Idoso
Alarminas/metabolismo
Feminino
Seres Humanos
Linfócitos do Interstício Tumoral/fisiologia
Masculino
Meia-Idade
Estudos Retrospectivos
Microambiente Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Alarmins); 0 (Histocompatibility Antigens Class I); 0 (MHC class I-related chain A); 0 (MICB antigen)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170908
[Lr] Data última revisão:
170908
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170614
[St] Status:MEDLINE
[do] DOI:10.1002/jso.24681


  7 / 96 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28596295
[Au] Autor:Pouwels SD; Faiz A; den Boef LE; Gras R; van den Berge M; Boezen HM; Korstanje R; Ten Hacken NHT; van Oosterhout AJM; Heijink IH; Nawijn MC
[Ad] Endereço:Department of Pathology and Medical Biology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands; s.d.pouwels@umcg.nl.
[Ti] Título:Genetic variance is associated with susceptibility for cigarette smoke-induced DAMP release in mice.
[So] Source:Am J Physiol Lung Cell Mol Physiol;313(3):L559-L580, 2017 Sep 01.
[Is] ISSN:1522-1504
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Chronic obstructive pulmonary disease (COPD) is characterized by unresolved neutrophilic airway inflammation and is caused by chronic exposure to toxic gases, such as cigarette smoke (CS), in genetically susceptible individuals. Recent data indicate a role for damage-associated molecular patterns (DAMPs) in COPD. Here, we investigated the genetics of CS-induced DAMP release in 28 inbred mouse strains. Subsequently, in lung tissue from a subset of strains, the expression of the identified candidate genes was analyzed. We tested whether small interfering RNA-dependent knockdown of candidate genes altered the susceptibility of the human A549 cell line to CS-induced cell death and DAMP release. Furthermore, we tested whether these genes were differentially regulated by CS exposure in bronchial brushings obtained from individuals with a family history indicative of either the presence or absence of susceptibility for COPD. We observed that, of the four DAMPs tested, double-stranded DNA (dsDNA) showed the highest correlation with neutrophilic airway inflammation. Genetic analyses identified 11 candidate genes governing either CS-induced or basal dsDNA release in mice. Two candidate genes ( and ) showed differential expression in lung tissue on CS exposure between susceptible and nonsusceptible mouse strains. Knockdown of and in A549 cells altered susceptibility to CS extract-induced cell death and DAMP release. In bronchial brushings, CS-induced expression of and was significantly different between individuals susceptible or nonsusceptible for COPD. Our study shows that genetic variance in a mouse model is associated with CS-induced DAMP release, and that this might contribute to susceptibility for COPD.
[Mh] Termos MeSH primário: Alarminas/metabolismo
Estudos de Associação Genética
Predisposição Genética para Doença
Variação Genética
Fumar/efeitos adversos
[Mh] Termos MeSH secundário: Animais
Líquido da Lavagem Broncoalveolar
Linhagem Celular
DNA/metabolismo
Regulação para Baixo/genética
Epitélio/metabolismo
Feminino
Haplótipos/genética
Seres Humanos
Contagem de Leucócitos
Camundongos
Polimorfismo de Nucleotídeo Único/genética
Doença Pulmonar Obstrutiva Crônica/genética
Doença Pulmonar Obstrutiva Crônica/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Alarmins); 9007-49-2 (DNA)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170610
[St] Status:MEDLINE
[do] DOI:10.1152/ajplung.00466.2016


  8 / 96 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28521686
[Au] Autor:Samara P; Karachaliou CE; Ioannou K; Papaioannou NE; Voutsas IF; Zikos C; Pirmettis I; Papadopoulos M; Kalbacher H; Livaniou E; Tsitsilonis OE; Voelter W
[Ad] Endereço:Section of Animal & Human Physiology, Department of Biology, National and Kapodistrian University of Athens, Panepistimiopolis, Athens 15784, Greece.
[Ti] Título:Prothymosin Alpha: An Alarmin and More...
[So] Source:Curr Med Chem;24(17):1747-1760, 2017.
[Is] ISSN:1875-533X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/OBJECTIVE: Prothymosin alpha (proTα) is a ubiquitous polypeptide first isolated by Haritos in 1984, whose role still remains partly elusive. We know that proTα acts both, intracellularly, as an anti-apoptotic and proliferation mediator, and extracellularly, as a biologic response modifier mediating immune responses similarly to molecules termed as "alarmins". Our research team pioneered the elucidation of the mechanisms underlying the observed activities of proTα. RESULTS: We were the first to demonstrate that proTα levels increase during normal and abnormal cell proliferation. We showed that proTα acts pleiotropically, inducing immunomodulatory effects on immune cell populations. We revealed that the immunoreactive region of proTα is the carboxyterminal decapeptide proTα(100-109) and both molecules stimulate innate immune responses, signaling through Toll-like receptors (TLRs), specifically TLR-4. We reported that proTα and proTα(100-109) bind on the surface of human neutrophils on sites involving TLR-4, and cell activation is complemented by cytoplasmic calcium ion influx. Further, we showed that proTα and proTα(100-109) act as adjuvants upstream of lymphocyte stimulation and, in the presence of antigen, promote the expansion of antigen-reactive effectors. Most recently, we reported that proTα(100-109) may accumulate in experimentally inflamed sites and can serve as a surrogate biomarker in severe bacterial infections, proposing that extracellular release of proTα or proTα(100- 109) alerts the immune system during conditions of danger. CONCLUSION: We, therefore, suggest that proTα, and likely proTα(100-109), act as alarmins, being important immune mediators as well as biomarkers, and could eventually become targets for new therapeutic/diagnostic approaches in immune-related diseases like cancer, inflammation, and sepsis.
[Mh] Termos MeSH primário: Alarminas/metabolismo
Precursores de Proteínas/metabolismo
Timosina/análogos & derivados
[Mh] Termos MeSH secundário: Alarminas/química
Doenças Autoimunes/metabolismo
Doenças Autoimunes/patologia
Seres Humanos
Imunidade Inata/efeitos dos fármacos
Células Matadoras Naturais/citologia
Neoplasias/tratamento farmacológico
Neoplasias/metabolismo
Neoplasias/patologia
Precursores de Proteínas/química
Precursores de Proteínas/uso terapêutico
Sepse/metabolismo
Sepse/patologia
Linfócitos T/citologia
Linfócitos T/efeitos dos fármacos
Linfócitos T/metabolismo
Timosina/química
Timosina/metabolismo
Timosina/uso terapêutico
Receptores Toll-Like/química
Receptores Toll-Like/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Alarmins); 0 (Protein Precursors); 0 (Toll-Like Receptors); 0 (prothymosin alpha); 61512-21-8 (Thymosin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170908
[Lr] Data última revisão:
170908
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170520
[St] Status:MEDLINE
[do] DOI:10.2174/0929867324666170518110033


  9 / 96 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28404746
[Au] Autor:Handly LN; Wollman R
[Ad] Endereço:Department of Chemistry and Biochemistry, University of California, Los Angeles, Los Angeles, CA 90095.
[Ti] Título:Wound-induced Ca wave propagates through a simple release and diffusion mechanism.
[So] Source:Mol Biol Cell;28(11):1457-1466, 2017 Jun 01.
[Is] ISSN:1939-4586
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Damage-associated molecular patterns (DAMPs) are critical mediators of information concerning tissue damage from damaged cells to neighboring healthy cells. ATP acts as an effective DAMP when released into extracellular space from damaged cells. Extracellular ATP receptors monitor tissue damage and activate a Ca wave in the surrounding healthy cells. How the Ca wave propagates through cells after a wound is unclear. Ca wave activation can occur extracellularly via external receptors or intracellularly through GAP junctions. Three potential mechanisms to propagate the Ca wave are source and sink, amplifying wave, and release and diffusion. Both source and sink and amplifying wave regulate ATP levels using hydrolysis or secretion, respectively, whereas release and diffusion relies on dilution. Here we systematically test these hypotheses using a microfluidics assay to mechanically wound an epithelial monolayer in combination with direct manipulation of ATP hydrolysis and release. We show that a release and diffusion model sufficiently explains Ca -wave propagation after an epithelial wound. A release and diffusion model combines the benefits of fast activation at short length scales with a self-limiting response to prevent unnecessary inflammatory responses harmful to the organism.
[Mh] Termos MeSH primário: Alarminas/metabolismo
Sinalização do Cálcio/fisiologia
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/metabolismo
Cálcio/metabolismo
Células Cultivadas
Difusão
Células Epiteliais/metabolismo
Células Epiteliais/fisiologia
Espaço Extracelular/metabolismo
Junções Comunicantes/metabolismo
Seres Humanos
Microfluídica/estatística & dados numéricos
Modelos Biológicos
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Alarmins); 8L70Q75FXE (Adenosine Triphosphate); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170414
[St] Status:MEDLINE
[do] DOI:10.1091/mbc.E16-10-0695


  10 / 96 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28394332
[Au] Autor:Shichita T; Ito M; Morita R; Komai K; Noguchi Y; Ooboshi H; Koshida R; Takahashi S; Kodama T; Yoshimura A
[Ad] Endereço:Department of Microbiology and Immunology, School of Medicine, Keio University, Tokyo, Japan.
[Ti] Título:MAFB prevents excess inflammation after ischemic stroke by accelerating clearance of damage signals through MSR1.
[So] Source:Nat Med;23(6):723-732, 2017 Jun.
[Is] ISSN:1546-170X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Damage-associated molecular patterns (DAMPs) trigger sterile inflammation after tissue injury, but the mechanisms underlying the resolution of inflammation remain unclear. In this study, we demonstrate that common DAMPs, such as high-mobility-group box 1 (HMGB1), peroxiredoxins (PRXs), and S100A8 and S100A9, were internalized through the class A scavenger receptors MSR1 and MARCO in vitro. In ischemic murine brain, DAMP internalization was largely mediated by MSR1. An elevation of MSR1 levels in infiltrating myeloid cells observed 3 d after experimental stroke was dependent on the transcription factor Mafb. Combined deficiency for Msr1 and Marco, or for Mafb alone, in infiltrating myeloid cells caused impaired clearance of DAMPs, more severe inflammation, and exacerbated neuronal injury in a murine model of ischemic stroke. The retinoic acid receptor (RAR) agonist Am80 increased the expression of Mafb, thereby enhancing MSR1 expression. Am80 exhibited therapeutic efficacy when administered, even at 24 h after the onset of experimental stroke. Our findings uncover cellular mechanisms contributing to DAMP clearance in resolution of the sterile inflammation triggered by tissue injury.
[Mh] Termos MeSH primário: Alarminas/imunologia
Encéfalo/imunologia
Infarto da Artéria Cerebral Média/imunologia
Fator de Transcrição MafB/imunologia
Células Mieloides/imunologia
Receptores Imunológicos/imunologia
Receptores Depuradores Classe A/imunologia
[Mh] Termos MeSH secundário: Animais
Benzoatos/farmacologia
Encéfalo/efeitos dos fármacos
Isquemia Encefálica/imunologia
Sistemas CRISPR-Cas
Calgranulina A/imunologia
Calgranulina B/imunologia
Imunoprecipitação da Cromatina
Proteína HMGB1/imunologia
Inflamação
Fator de Transcrição MafB/efeitos dos fármacos
Fator de Transcrição MafB/genética
Camundongos
Células Mieloides/metabolismo
Peroxirredoxinas/imunologia
Receptores Imunológicos/genética
Receptores do Ácido Retinoico/agonistas
Receptores Depuradores Classe A/efeitos dos fármacos
Receptores Depuradores Classe A/genética
Acidente Vascular Cerebral/imunologia
Tetra-Hidronaftalenos/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Alarmins); 0 (Benzoates); 0 (Calgranulin A); 0 (Calgranulin B); 0 (HMGB1 Protein); 0 (HMGB1 protein, mouse); 0 (MafB Transcription Factor); 0 (Mafb protein, mouse); 0 (Marco protein, mouse); 0 (Msr1 protein, mouse); 0 (Receptors, Immunologic); 0 (Receptors, Retinoic Acid); 0 (S100A9 protein, mouse); 0 (S100a8 protein, mouse); 0 (Scavenger Receptors, Class A); 0 (Tetrahydronaphthalenes); 08V52GZ3H9 (tamibarotene); EC 1.11.1.15 (Peroxiredoxins)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170829
[Lr] Data última revisão:
170829
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170411
[St] Status:MEDLINE
[do] DOI:10.1038/nm.4312



página 1 de 10 ir para página                        
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde