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[PMID]:29267673
[Au] Autor:Yan Y; Qi S; Gong SQ; Shang G; Zhao Y
[Ad] Endereço:Tongji University, Shanghai Engineering Research Center of Tooth Restoration and Regeneration, Department of Pediatric Dentistry, Shanghai, China.
[Ti] Título:Effect of CRABP2 on the proliferation and odontoblastic differentiation of hDPSCs.
[So] Source:Braz Oral Res;31:e112, 2017 Dec 18.
[Is] ISSN:1807-3107
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:Cellular retinoic acid-binding protein 2 (CRABP2) has been detected in several organs during embryonic development. Recent studies have demonstrated that CRABP2 plays important roles in the retinoic acid, ß-catenin and Notch signaling pathways, as well as in the interaction between epithelial and mesenchymal cells, which are important for human dental pulp stem cells (hDPSCs) and tooth development. In the present study, the expression of CRABP2 during mouse molar development and the role of CRABP2 in hDPSC odontoblastic differentiation were evaluated. CRABP2 was gradually decreased during the development of the first maxillary molar, which exhibited the same trend as the expression of CRABP2 during the odontoblastic induction of hDPSCs. CRABP2 knockdown inhibited the proliferative ability of hDPSCs, while it enhanced odontoblastic differentiation via promoting mineralization nodule formation and upregulating the activity of alkaline phosphatase and the expression of mineralization-related genes. The present study uncovered a novel function of CRABP2 in hDPSCs. Our data suggest that CRABP2 may act as a regulator during the proliferation and differentiation of hDPSCs.
[Mh] Termos MeSH primário: Diferenciação Celular/fisiologia
Proliferação Celular/fisiologia
Polpa Dentária/citologia
Odontoblastos/fisiologia
Receptores do Ácido Retinoico/fisiologia
Células-Tronco/fisiologia
[Mh] Termos MeSH secundário: Fosfatase Alcalina
Análise de Variância
Animais
Antraquinonas
Western Blotting
Comunicação Celular
Células Cultivadas
Corantes
Regulação para Baixo/fisiologia
Feminino
Seres Humanos
Imuno-Histoquímica
Masculino
Camundongos Endogâmicos C57BL
Receptores do Ácido Retinoico/análise
Valores de Referência
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anthraquinones); 0 (Coloring Agents); 0 (Receptors, Retinoic Acid); 0 (retinoic acid binding protein II, cellular); 60MEW57T9G (alizarin); EC 3.1.3.1 (Alkaline Phosphatase)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE


  2 / 29180 MEDLINE  
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[PMID]:28453731
[Au] Autor:Demolli S; Doddaballapur A; Devraj K; Stark K; Manavski Y; Eckart A; Zehendner CM; Lucas T; Korff T; Hecker M; Massberg S; Liebner S; Kaluza D; Boon RA; Dimmeler S
[Ad] Endereço:Institute for Cardiovascular Regeneration, Centre of Molecular Medicine, Goethe University, Theodor Stern Kai 7, 60590 Frankfurt, Germany.
[Ti] Título:Shear stress-regulated miR-27b controls pericyte recruitment by repressing SEMA6A and SEMA6D.
[So] Source:Cardiovasc Res;113(6):681-691, 2017 May 01.
[Is] ISSN:1755-3245
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Aims: Vessel maturation involves the recruitment of mural cells such as pericytes and smooth muscle cells. Laminar shear stress is a major trigger for vessel maturation, but the molecular mechanisms by which shear stress affects recruitment of pericytes are unclear. MicroRNAs (miRs) are small non-coding RNAs, which post-transcriptionally control gene expression. The aim of the present study was to unveil the mechanism by which shear stress-regulated microRNAs contribute to vessel maturation. Methods and results: Here, we show that laminar shear stress increased miR-27a and miR-27b expression in vitro and in ex vivo in mouse femoral artery explants. Overexpression of miR-27b in endothelial cells increased pericyte adhesion and pericyte recruitment in vitro. In vitro barrier function of endothelial-pericyte co-cultures was augmented by miR-27b overexpression, whereas inhibition of miR-27a/b reduced adhesion and pericyte coverage and decreased barrier functions. In vivo, pharmacological inhibition of miR-27a/b by locked nucleic acid antisense oligonucleotides significantly reduced pericyte coverage and increased water content in the murine uterus. MiR-27b overexpression repressed semaphorins (SEMA), which mediate repulsive signals, and the vessel destabilizing human but not mouse Angiopoietin-2 (Ang-2). Silencing of SEMA6A and SEMA6D rescued the reduced pericyte adhesion by miR-27 inhibition. Furthermore, inhibition of SEMA6D increased barrier function of an endothelial-pericyte co-culture in vitro. Conclusion: The present study demonstrates for the first time that shear stress-regulated miR-27b promotes the interaction of endothelial cells with pericytes, partly by repressing SEMA6A and SEMA6D.
[Mh] Termos MeSH primário: Encéfalo/irrigação sanguínea
Comunicação Celular
Movimento Celular
Células Endoteliais/metabolismo
Mecanotransdução Celular
Microvasos/metabolismo
Pericitos/metabolismo
Semaforinas/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Técnicas de Cocultura
Células Endoteliais da Veia Umbilical Humana/metabolismo
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
MicroRNAs/genética
MicroRNAs/metabolismo
Interferência de RNA
Semaforinas/genética
Estresse Mecânico
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MIRN27 microRNA, human); 0 (MicroRNAs); 0 (Mirn27 microRNA, mouse); 0 (SEMA6A protein, human); 0 (Sema6a protein, mouse); 0 (Sema6d protein, mouse); 0 (Semaphorins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1093/cvr/cvx032


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[PMID]:28464904
[Au] Autor:Bardeesi ASA; Gao J; Zhang K; Yu S; Wei M; Liu P; Huang H
[Ad] Endereço:Zhongshan Medical School, Sun Yat-sen University, Guangzhou, China.
[Ti] Título:A novel role of cellular interactions in vascular calcification.
[So] Source:J Transl Med;15(1):95, 2017 May 03.
[Is] ISSN:1479-5876
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A series of clinical trials have confirmed the correlation between vascular calcification (VC) and cardiovascular events and mortality. However, current treatments have little effects on the regression of VC. Potent and illustrative mechanisms have been proven to exist in both bone metabolism and VC, indicating that these two processes share similarities in onset and progression. Multiple osteoblast-like cells and signaling pathways are involved in the process of VC. In this review, we summarized the roles of different osteoblast-like cells and we emphasized on how they communicated and interacted with each other using different signaling pathways. Further studies are needed to uncover the underlying mechanisms and to provide novel therapies for VC.
[Mh] Termos MeSH primário: Comunicação Celular
Calcificação Vascular/patologia
[Mh] Termos MeSH secundário: Animais
Células Endoteliais/patologia
Seres Humanos
Osteoblastos/patologia
Transdução de Sinais
Células-Tronco/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[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:170504
[St] Status:MEDLINE
[do] DOI:10.1186/s12967-017-1190-z


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[PMID]:28467294
[Au] Autor:van der Pol E; Harrison P
[Ad] Endereço:a Biomedical Engineering & Physics , Academic Medical Centre, University of Amsterdam , Amsterdam , The Netherlands.
[Ti] Título:From platelet dust to gold dust: physiological importance and detection of platelet microvesicles.
[So] Source:Platelets;28(3):211-213, 2017 05.
[Is] ISSN:1369-1635
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Plaquetas/química
Micropartículas Derivadas de Células/metabolismo
Integrina beta3/genética
Trombose/fisiopatologia
[Mh] Termos MeSH secundário: Transporte Biológico/fisiologia
Biomarcadores/metabolismo
Plaquetas/ultraestrutura
Comunicação Celular/fisiologia
Micropartículas Derivadas de Células/genética
Micropartículas Derivadas de Células/ultraestrutura
Expressão Gênica
Ouro/química
Seres Humanos
Imuno-Histoquímica
Integrina beta3/metabolismo
Nanopartículas Metálicas/química
Tamanho da Partícula
Ativação Plaquetária/fisiologia
Trombose/genética
Trombose/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Biomarkers); 0 (ITGB3 protein, human); 0 (Integrin beta3); 7440-57-5 (Gold)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1080/09537104.2017.1282781


  5 / 29180 MEDLINE  
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[PMID]:29386430
[Au] Autor:Hanawa T; Kawano Y; Satoh M
[Ad] Endereço:Faculty of Pharmaceutical Sciences, Tokyo University of Science.
[Ti] Título:[Development of "Patient Friendly Formulations" to Counter the Side Effects of Cancer Chemotherapy].
[So] Source:Yakugaku Zasshi;138(2):169-175, 2018.
[Is] ISSN:1347-5231
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo: Anticancer drug-induced stomatitis develops in 30% to 40% of cancer patients undergoing chemotherapy. However, medications for this condition are not commercially available in Japan. The "hospital formulation" is a customized medicine which hospital pharmacists prepare when doctors cannot carry out the medical therapy most suitable for a patient using commercial medicines. However, as the duties of pharmacists increase, use of the "hospital fomulation" decreases. Therefore, development of "hospital fomulations" based on individual evidence has a limit. Irsogladine maleate (IM) is a drug with gastric mucosal protective properties. IM increases intracellular cAMP levels in the gastric mucosa and activates communication between cells. It has been reported that the oral administration of IM reduces the incidence of 5-FU-based chemotherapy-induced stomatitis. However, there have been no reports on the effect of the direct use of IM in treating stomatitis. Therefore, we studied the development of an IM oral spray for stomatitis treatment, and obtained evidence of a direct effect in an animal experiment using a stomatitis model. Next, rebamipide mouthwash was administered to patients who had stomatitis caused by cancer chemotherapy. The total scores were classified into Grades 0 to 4 and evaluated as a stomatitis evaluation score (SES). When comparing SES and changes in the stomatitis area in patients, gradual reductions in the extent of stomatitis were observed, even during the period when SES did not change. Having patients fill in an observation chart was effective for grasping changes in symptoms in outpatients.
[Mh] Termos MeSH primário: Alanina/análogos & derivados
Antineoplásicos/efeitos adversos
Composição de Medicamentos
Quinolonas/administração & dosagem
Estomatite/induzido quimicamente
Estomatite/tratamento farmacológico
Triazinas/administração & dosagem
Triazinas/farmacologia
[Mh] Termos MeSH secundário: Administração Oral
Alanina/administração & dosagem
Animais
Comunicação Celular/efeitos dos fármacos
AMP Cíclico/metabolismo
Modelos Animais de Doenças
Medicina Baseada em Evidências
Mucosa Gástrica/citologia
Mucosa Gástrica/metabolismo
Seres Humanos
Antissépticos Bucais
Estomatite/prevenção & controle
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Mouthwashes); 0 (Quinolones); 0 (Triazines); E0399OZS9N (Cyclic AMP); LR583V32ZR (rebamipide); OF5P57N2ZX (Alanine); QBX79NZC1D (irsogladine)
[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.17-00174-2


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[PMID]:27773427
[Au] Autor:Gewin L; Zent R; Pozzi A
[Ad] Endereço:Division of Nephrology, Department of Medicine, Vanderbilt Medical Center, Nashville, Tennessee, USA; Department of Cell and Developmental Biology, Vanderbilt Medical Center, Nashville, Tennessee, USA; Veterans Affairs Medical Center, Nashville, Tennessee, USA.
[Ti] Título:Progression of chronic kidney disease: too much cellular talk causes damage.
[So] Source:Kidney Int;91(3):552-560, 2017 Mar.
[Is] ISSN:1523-1755
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tubulointerstitial fibrosis, tubular atrophy, and peritubular capillary rarefaction are major hallmarks of chronic kidney disease. The tubulointerstitium consists of multiple cell components including tubular epithelial, mesenchymal (fibroblasts and pericytes), endothelial, and inflammatory cells. Crosstalk among these cell components is a key component in the pathogenesis of this complex disease. After severe or recurrent injury, the renal tubular epithelial cells undergo changes in structure and cell cycle that are accompanied by altered expression and production of cytokines. These cytokines contribute to the initiation of the fibrotic response by favoring activation of fibroblasts, recruitment of inflammatory cells, and loss of endothelial cells. This review focuses on how augmented growth factor and cytokine production induces epithelial crosstalk with cells in the interstitium to promote progressive tubulointerstitial fibrosis after renal injury.
[Mh] Termos MeSH primário: Comunicação Celular
Citocinas/metabolismo
Rim/metabolismo
Insuficiência Renal Crônica/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Citocinas/imunologia
Fibrose
Seres Humanos
Rim/imunologia
Rim/patologia
Insuficiência Renal Crônica/imunologia
Insuficiência Renal Crônica/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cytokines)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


  7 / 29180 MEDLINE  
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[PMID]:29352112
[Au] Autor:Furuya M; Kikuta J; Fujimori S; Seno S; Maeda H; Shirazaki M; Uenaka M; Mizuno H; Iwamoto Y; Morimoto A; Hashimoto K; Ito T; Isogai Y; Kashii M; Kaito T; Ohba S; Chung UI; Lichtler AC; Kikuchi K; Matsuda H; Yoshikawa H; Ishii M
[Ad] Endereço:Department of Immunology and Cell Biology, Graduate School of Medicine & Frontier Biosciences, Osaka University, Osaka, 565-0871, Japan.
[Ti] Título:Direct cell-cell contact between mature osteoblasts and osteoclasts dynamically controls their functions in vivo.
[So] Source:Nat Commun;9(1):300, 2018 01 19.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Bone homeostasis is regulated by communication between bone-forming mature osteoblasts (mOBs) and bone-resorptive mature osteoclasts (mOCs). However, the spatial-temporal relationship and mode of interaction in vivo remain elusive. Here we show, by using an intravital imaging technique, that mOB and mOC functions are regulated via direct cell-cell contact between these cell types. The mOBs and mOCs mainly occupy discrete territories in the steady state, although direct cell-cell contact is detected in spatiotemporally limited areas. In addition, a pH-sensing fluorescence probe reveals that mOCs secrete protons for bone resorption when they are not in contact with mOBs, whereas mOCs contacting mOBs are non-resorptive, suggesting that mOBs can inhibit bone resorption by direct contact. Intermittent administration of parathyroid hormone causes bone anabolic effects, which lead to a mixed distribution of mOBs and mOCs, and increase cell-cell contact. This study reveals spatiotemporal intercellular interactions between mOBs and mOCs affecting bone homeostasis in vivo.
[Mh] Termos MeSH primário: Reabsorção Óssea/diagnóstico por imagem
Comunicação Celular/fisiologia
Osteoblastos/citologia
Osteoclastos/citologia
Osteogênese/fisiologia
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Feminino
Corantes Fluorescentes/química
Expressão Gênica
Genes Reporter
Proteínas de Fluorescência Verde/genética
Proteínas de Fluorescência Verde/metabolismo
Homeostase/fisiologia
Concentração de Íons de Hidrogênio
Microscopia Intravital/métodos
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Osteoblastos/efeitos dos fármacos
Osteoblastos/fisiologia
Osteoclastos/efeitos dos fármacos
Osteoclastos/fisiologia
Hormônio Paratireóideo/farmacologia
Cultura Primária de Células
Crânio/citologia
Crânio/diagnóstico por imagem
Crânio/efeitos dos fármacos
Crânio/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Fluorescent Dyes); 0 (Parathyroid Hormone); 0 (enhanced green fluorescent protein); 147336-22-9 (Green Fluorescent Proteins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180121
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02541-w


  8 / 29180 MEDLINE  
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[PMID]:29335551
[Au] Autor:Fang T; Lv H; Lv G; Li T; Wang C; Han Q; Yu L; Su B; Guo L; Huang S; Cao D; Tang L; Tang S; Wu M; Yang W; Wang H
[Ad] Endereço:International Co-operation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Institute, Second Military Medical University, Shanghai, 200438, China.
[Ti] Título:Tumor-derived exosomal miR-1247-3p induces cancer-associated fibroblast activation to foster lung metastasis of liver cancer.
[So] Source:Nat Commun;9(1):191, 2018 01 15.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The communication between tumor-derived elements and stroma in the metastatic niche has a critical role in facilitating cancer metastasis. Yet, the mechanisms tumor cells use to control metastatic niche formation are not fully understood. Here we report that in the lung metastatic niche, high-metastatic hepatocellular carcinoma (HCC) cells exhibit a greater capacity to convert normal fibroblasts to cancer-associated fibroblasts (CAFs) than low-metastatic HCC cells. We show high-metastatic HCC cells secrete exosomal miR-1247-3p that directly targets B4GALT3, leading to activation of ß1-integrin-NF-κB signaling in fibroblasts. Activated CAFs further promote cancer progression by secreting pro-inflammatory cytokines, including IL-6 and IL-8. Clinical data show high serum exosomal miR-1247-3p levels correlate with lung metastasis in HCC patients. These results demonstrate intercellular crosstalk between tumor cells and fibroblasts is mediated by tumor-derived exosomes that control lung metastasis of HCC, providing potential targets for prevention and treatment of cancer metastasis.
[Mh] Termos MeSH primário: Fibroblastos Associados a Câncer/metabolismo
Carcinoma Hepatocelular/metabolismo
Exossomos/metabolismo
Regulação Neoplásica da Expressão Gênica
Neoplasias Hepáticas/metabolismo
Neoplasias Pulmonares/metabolismo
MicroRNAs/genética
N-Acetil-Lactosamina Sintase/genética
[Mh] Termos MeSH secundário: Animais
Fibroblastos Associados a Câncer/patologia
Carcinoma Hepatocelular/genética
Carcinoma Hepatocelular/secundário
Comunicação Celular
Linhagem Celular Tumoral
Transformação Celular Neoplásica/genética
Transformação Celular Neoplásica/patologia
Exossomos/química
Seres Humanos
Integrina beta1/genética
Integrina beta1/metabolismo
Interleucina-6/genética
Interleucina-6/metabolismo
Interleucina-8/genética
Interleucina-8/metabolismo
Neoplasias Hepáticas/genética
Neoplasias Hepáticas/patologia
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/secundário
Masculino
Camundongos
Camundongos Nus
MicroRNAs/secreção
N-Acetil-Lactosamina Sintase/metabolismo
Invasividade Neoplásica
Transplante de Neoplasias
Células Neoplásicas Circulantes/metabolismo
Células Neoplásicas Circulantes/patologia
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (IL6 protein, human); 0 (Integrin beta1); 0 (Interleukin-6); 0 (Interleukin-8); 0 (MIRN1247 microRNA, human); 0 (MicroRNAs); EC 2.4.1.90 (N-Acetyllactosamine Synthase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180117
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02583-0


  9 / 29180 MEDLINE  
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[PMID]:29254286
[Au] Autor:Robuffo I; Toniato E; Tettamanti L; Mastrangelo F; Ronconi G; Frydas I; Caraffa A; Kritas SK; Conti P
[Ad] Endereço:Institute of Molecular Genetics, CNR, Sede di Chieti, Italy.
[Ti] Título:Mast cell in innate immunity mediated by proinflammatory and antiinflammatory IL-1 family members.
[So] Source:J Biol Regul Homeost Agents;31(4):837-842, 2017 Oct-Dec.
[Is] ISSN:0393-974X
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:Innate immunity consists of physical and chemical barriers which provide the early defense against infections. Innate immunity orchestrates the defense of the host with cellular and biochemical proteins. Mast cells (MCs) are involved in innate and adaptive immunity and are the first line of defense which generates multiple inflammatory cytokines/chemokines in response to numerous antigens. MC-activated antigen receptor Fc-RI provokes a number of important biochemical pathways with secretion of numerous vasoactive, chemoattractant and inflammatory compounds which participate in allergic and inflammatory diseases. MCs can also be activated by Th1 cytokines and generate pre-formed and de novo inflammatory mediators, including TNF. IL-37 is an anti-inflammatory cytokine which binds IL-18R-alpha chain and reduces the production of inflammatory IL-1 family members. IL-37 down-regulates innate immunity by inhibiting macrophage response and its accumulation and reduces the cytokines that mediate inflammatory diseases. Here, we discuss the relationship between MCs, innate immunity, and pro-inflammatory and anti-inflammatory cytokines.
[Mh] Termos MeSH primário: Inflamação/imunologia
Interleucina-1/imunologia
Macrófagos/imunologia
Mastócitos/imunologia
Receptores de Interleucina-1/imunologia
[Mh] Termos MeSH secundário: Imunidade Adaptativa
Linfócitos B/imunologia
Linfócitos B/patologia
Comunicação Celular
Regulação da Expressão Gênica
Seres Humanos
Imunidade Inata
Inflamação/genética
Inflamação/patologia
Interleucina-1/genética
Subunidade alfa de Receptor de Interleucina-18/genética
Subunidade alfa de Receptor de Interleucina-18/imunologia
Peptídeos e Proteínas de Sinalização Intracelular/genética
Peptídeos e Proteínas de Sinalização Intracelular/imunologia
Macrófagos/patologia
Mastócitos/patologia
Receptores de Interleucina-1/genética
Transdução de Sinais
Linfócitos T/imunologia
Linfócitos T/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (FcRI protein, human); 0 (IL18R1 protein, human); 0 (IL37 protein, human); 0 (Interleukin-1); 0 (Interleukin-18 Receptor alpha Subunit); 0 (Intracellular Signaling Peptides and Proteins); 0 (Receptors, Interleukin-1)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171220
[St] Status:MEDLINE


  10 / 29180 MEDLINE  
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[PMID]:29173353
[Au] Autor:Ratajczak MZ; Ratajczak J
[Ad] Endereço:Department of Medicine, Stem Cell Institute at James Graham Brown Cancer Center, University of Louisville, Louisville, Kentucky. Electronic address: mzrata01@louisville.edu.
[Ti] Título:Extracellular Microvesicles as Game Changers in Better Understanding the Complexity of Cellular Interactions-From Bench to Clinical Applications.
[So] Source:Am J Med Sci;354(5):449-452, 2017 11.
[Is] ISSN:1538-2990
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Recent research has led to wide acceptance and better understanding of a novel mechanism for cell-cell communication that employs a network of extracellular microvesicles (ExMVs). Derived from the plasma membrane or the endosomal membrane compartment, these small, spherical membrane fragments are secreted from the cell surface or in the process of exocytosis from endosomal membrane compartment and (1) with ligands expressed on their surface directly stimulate target cells in a paracrine manner, (2) transfer cell membrane receptors to target cells or (3) deliver encapsulated messenger RNA, microRNA, proteins and bioactive lipids to target cells. This represents an evolutionarily ancient mechanism by which cells signal their presence in the microenvironment, communicate with each other and affect the biology of neighboring cells. Evidence suggests the pivotal role of ExMVs in almost all biological processes within the body as well as their involvement in certain pathologies. Moreover, liquid biopsies based on deciphering the molecular signature of ExMVs promise to revolutionize laboratory diagnostics. At the same time, there are ongoing attempts to employ them as delivery vehicles for drugs as well as therapeutics in regenerative medicine, oncology and immunotherapy.
[Mh] Termos MeSH primário: Comunicação Celular
Vesículas Extracelulares/metabolismo
MicroRNAs/metabolismo
Comunicação Parácrina
RNA Mensageiro/metabolismo
[Mh] Termos MeSH secundário: Seres Humanos
Ligantes
Proteínas/metabolismo
Receptores Citoplasmáticos e Nucleares/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Ligands); 0 (MicroRNAs); 0 (Proteins); 0 (RNA, Messenger); 0 (Receptors, Cytoplasmic and Nuclear)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE



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