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Pesquisa : A11.148.378.590 [Categoria DeCS]
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[PMID]:29300724
[Au] Autor:Draper JE; Sroczynska P; Fadlullah MZH; Patel R; Newton G; Breitwieser W; Kouskoff V; Lacaud G
[Ad] Endereço:Cancer Research UK Stem Cell Biology Group, Cancer Research UK Manchester Institute, Manchester Cancer Research Centre, The University of Manchester, Manchester, United Kingdom.
[Ti] Título:A novel prospective isolation of murine fetal liver progenitors to study in utero hematopoietic defects.
[So] Source:PLoS Genet;14(1):e1007127, 2018 01.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In recent years, highly detailed characterization of adult bone marrow (BM) myeloid progenitors has been achieved and, as a result, the impact of somatic defects on different hematopoietic lineage fate decisions can be precisely determined. Fetal liver (FL) hematopoietic progenitor cells (HPCs) are poorly characterized in comparison, potentially hindering the study of the impact of genetic alterations on midgestation hematopoiesis. Numerous disorders, for example infant acute leukemias, have in utero origins and their study would therefore benefit from the ability to isolate highly purified progenitor subsets. We previously demonstrated that a Runx1 distal promoter (P1)-GFP::proximal promoter (P2)-hCD4 dual-reporter mouse (Mus musculus) model can be used to identify adult BM progenitor subsets with distinct lineage preferences. In this study, we undertook the characterization of the expression of Runx1-P1-GFP and P2-hCD4 in FL. Expression of P2-hCD4 in the FL immunophenotypic Megakaryocyte-Erythroid Progenitor (MEP) and Common Myeloid Progenitor (CMP) compartments corresponded to increased granulocytic/monocytic/megakaryocytic and decreased erythroid specification. Moreover, Runx1-P2-hCD4 expression correlated with several endogenous cell surface markers' expression, including CD31 and CD45, providing a new strategy for prospective identification of highly purified fetal myeloid progenitors in transgenic mouse models. We utilized this methodology to compare the impact of the deletion of either total RUNX1 or RUNX1C alone and to determine the fetal HPCs lineages most substantially affected. This new prospective identification of FL progenitors therefore raises the prospect of identifying the underlying gene networks responsible with greater precision than previously possible.
[Mh] Termos MeSH primário: Linhagem da Célula/genética
Células-Tronco Hematopoéticas/citologia
Células Progenitoras Mieloides/citologia
[Mh] Termos MeSH secundário: Animais
Medula Óssea/embriologia
Diferenciação Celular
Subunidade alfa 2 de Fator de Ligação ao Core/genética
Subunidade alfa 2 de Fator de Ligação ao Core/metabolismo
Modelos Animais de Doenças
Granulócitos/citologia
Hematopoese/genética
Células-Tronco Hematopoéticas/metabolismo
Seres Humanos
Fígado/citologia
Fígado/embriologia
Fígado/metabolismo
Megacariócitos/citologia
Camundongos
Camundongos Transgênicos
Monócitos/citologia
Estudos Prospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Core Binding Factor Alpha 2 Subunit); 0 (Runx1 protein, mouse)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180128
[Lr] Data última revisão:
180128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180105
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1007127


  2 / 912 MEDLINE  
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[PMID]:28976973
[Au] Autor:Qin Y; Wu L; Ouyang Y; Zhou P; Zhou H; Wang Y; Ma J; Zhang J; Chen Y; Qian J; Tang Y; Shen N
[Ad] Endereço:Department of Rheumatology and Shanghai Institute of Rheumatology, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
[Ti] Título:MiR-125a Is a critical modulator for neutrophil development.
[So] Source:PLoS Genet;13(10):e1007027, 2017 Oct.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:MicroRNAs are universal post-transcriptional regulators in genomes. They have the ability of buffering gene expressional programs, contributing to robustness of biological systems and playing important roles in development, physiology and diseases. Here, we identified a microRNA, miR-125a, as a positive regulator of granulopoiesis. MiR125a knockout mice show reduced infiltration of neutrophils in the lung and alleviated tissue destruction after endotoxin challenge as a consequence of decreased neutrophil numbers. Furthermore, we demonstrated that this significant reduction of neutrophils was due to impaired development of granulocyte precursors to mature neutrophils in an intrinsic manner. We showed that Socs3, a critical repressor for granulopoiesis, was a target of miR-125a. Overall, our study revealed a new microRNA regulating granulocyte development and supported a model in which miR-125a acted as a fine-tuner of granulopoiesis.
[Mh] Termos MeSH primário: Leucopoese/genética
Leucopoese/fisiologia
MicroRNAs/genética
MicroRNAs/metabolismo
Neutrófilos/citologia
Neutrófilos/metabolismo
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Animais
Sítios de Ligação/genética
Morte Celular
Diferenciação Celular
Proliferação Celular
Fator Estimulador de Colônias de Granulócitos/metabolismo
Granulócitos/citologia
Granulócitos/metabolismo
Camundongos
Camundongos Knockout
Modelos Biológicos
Células Progenitoras Mieloides/citologia
Células Progenitoras Mieloides/metabolismo
Choque Séptico/genética
Choque Séptico/metabolismo
Choque Séptico/patologia
Transdução de Sinais
Proteína 3 Supressora da Sinalização de Citocinas/genética
Proteína 3 Supressora da Sinalização de Citocinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (MicroRNAs); 0 (Mirn125 microRNA, mouse); 0 (Socs3 protein, mouse); 0 (Suppressor of Cytokine Signaling 3 Protein); 143011-72-7 (Granulocyte Colony-Stimulating Factor)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171005
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1007027


  3 / 912 MEDLINE  
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[PMID]:28934717
[Au] Autor:Dai J; Kumbhare A; Youssef D; Yao ZQ; McCall CE; El Gazzar M
[Ad] Endereço:Department of Internal Medicine, East Tennessee State University College of Medicine, Johnson City, TN 37614, United States.
[Ti] Título:Expression of C/EBPß in myeloid progenitors during sepsis promotes immunosuppression.
[So] Source:Mol Immunol;91:165-172, 2017 11.
[Is] ISSN:1872-9142
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Sepsis-induced myeloid-derived suppressor cells (MDSCs) contribute to immunosuppression associated with sepsis. We reported that the CCAAT enhancer-binding protein C/EBPß activates microRNA (miR)-21 and miR-181b expressions, which induce transcription factor NFI-A to support the generation and expansion of MDSCs in the bone marrow and spleens of septic mice. Here, using a conditional knockout mouse model lacking C/EBPß in the myeloid lineage, we find that without C/EBPß, myeloid progenitor cells could not express miR-21 or miR-181b, and ectopic expression of C/EBPß in the C/EBPß-deficient myeloid progenitors activated the expression of the two miRNAs. Moreover, C/EBPß-reconstituted myeloid cells expressed IL-10 and reduced T cell proliferation and function, similar to control MDSCs that express C/EBPß. Exogenous expression of miR-21 and miR-181b in the C/EBPß-deficient myeloid progenitors from septic mice produced similar results. Notably, NFI-A-dependent transactivation of NF-kB MDSC generating pathway was reversed in the C/EBPß-deficient myeloid progenitors from septic mice. Together, these results support that decreasing C/EBPß expression prevents MDSC generation and decreases immunosuppression in septic mice, providing a target for sepsis treatment.
[Mh] Termos MeSH primário: Proteína beta Intensificadora de Ligação a CCAAT/imunologia
Regulação da Expressão Gênica/imunologia
Tolerância Imunológica
Interleucina-10/imunologia
Células Progenitoras Mieloides/imunologia
Sepse/imunologia
[Mh] Termos MeSH secundário: Animais
Proteína beta Intensificadora de Ligação a CCAAT/genética
Proliferação Celular/genética
Regulação da Expressão Gênica/genética
Interleucina-10/genética
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Knockout
MicroRNAs/genética
MicroRNAs/imunologia
Células Progenitoras Mieloides/patologia
NF-kappa B/genética
NF-kappa B/imunologia
Fatores de Transcrição NFI/genética
Fatores de Transcrição NFI/imunologia
Sepse/genética
Sepse/patologia
Linfócitos T/imunologia
Linfócitos T/patologia
Ativação Transcricional/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (CCAAT-Enhancer-Binding Protein-beta); 0 (Cebpb protein, mouse); 0 (IL10 protein, mouse); 0 (MIRN21 microRNA, mouse); 0 (MicroRNAs); 0 (NF-kappa B); 0 (NFI Transcription Factors); 0 (Nfia protein, mouse); 0 (mirn181 microRNA, mouse); 130068-27-8 (Interleukin-10)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171120
[Lr] Data última revisão:
171120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170922
[St] Status:MEDLINE


  4 / 912 MEDLINE  
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[PMID]:28717098
[Au] Autor:Goto K; Goto M; Ando-Imaoka M; Kai K; Mori K
[Ad] Endereço:Medicinal Safety Research Laboratories, Daiichi Sankyo Co., Ltd.
[Ti] Título:Evaluation of drug-induced hematotoxicity using novel in vitro monkey CFU-GM and BFU-E colony assays.
[So] Source:J Toxicol Sci;42(4):397-405, 2017.
[Is] ISSN:1880-3989
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:In order to evaluate drug-induced hematotoxicity in monkey cells in vitro, colony-forming unit-granulocyte, macrophage (CFU-GM), and burst-forming unit-erythroid (BFU-E) colony assays were established using mononuclear cells in the bone marrow collected from male cynomolgus monkeys. Furthermore, the effects of doxorubicin, chloramphenicol, and linezolid on CFU-GM and BFU-E colony formation were investigated using established monkey CFU-GM and BFU-E colony assays in comparison with those on human CFU-GM and BFU-E colonies acquired from human umbilical cord blood cells. Bone marrow mononuclear cells were collected from the ischial or iliac bone of male cynomolgus monkeys. The cells were subsequently processed by density gradient separation at 1.067, 1.070, or 1.077 g/mL for CFU-GM or 1.077 g/mL for BFU-E, and then cultured in methylcellulose medium for 9 or 13 days, respectively. A sufficient number of CFU-GM colonies were formed from mononuclear cells processed at a density of 1.070 g/mL. Moreover, the number of BFU-E colonies from the cells processed at a density of 1.077 g/mL was sufficient for the colony assay. The number of CFU-GM or BFU-E colonies decreased after treatment with the drugs of interest in a concentration-dependent manner. Compared with human CFU-GM, monkey CFU-GM were more sensitive to chloramphenicol and resistant to doxorubicin, whereas monkey BFU-E were more sensitive to all compounds in comparison to the sensitivity of human BFU-E. In conclusion, monkey CFU-GM and BFU-E colony assays were established and considered useful tools to evaluate the differences in drug-induced hematotoxicity between species.
[Mh] Termos MeSH primário: Cloranfenicol/toxicidade
Doxorrubicina/toxicidade
Linezolida/toxicidade
Células Progenitoras Mieloides/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Células da Medula Óssea/citologia
Células Cultivadas
Ensaio de Unidades Formadoras de Colônias
Relação Dose-Resposta a Droga
Sangue Fetal/citologia
Seres Humanos
Macaca fascicularis
Masculino
Especificidade da Espécie
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
66974FR9Q1 (Chloramphenicol); 80168379AG (Doxorubicin); ISQ9I6J12J (Linezolid)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171005
[Lr] Data última revisão:
171005
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170719
[St] Status:MEDLINE
[do] DOI:10.2131/jts.42.397


  5 / 912 MEDLINE  
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[PMID]:28658204
[Au] Autor:Shlush LI; Mitchell A; Heisler L; Abelson S; Ng SWK; Trotman-Grant A; Medeiros JJF; Rao-Bhatia A; Jaciw-Zurakowsky I; Marke R; McLeod JL; Doedens M; Bader G; Voisin V; Xu C; McPherson JD; Hudson TJ; Wang JCY; Minden MD; Dick JE
[Ad] Endereço:Princess Margaret Cancer Centre, University Health Network, Toronto, Ontario M5G 2M9, Canada.
[Ti] Título:Tracing the origins of relapse in acute myeloid leukaemia to stem cells.
[So] Source:Nature;547(7661):104-108, 2017 07 06.
[Is] ISSN:1476-4687
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In acute myeloid leukaemia, long-term survival is poor as most patients relapse despite achieving remission. Historically, the failure of therapy has been thought to be due to mutations that produce drug resistance, possibly arising as a consequence of the mutagenic properties of chemotherapy drugs. However, other lines of evidence have pointed to the pre-existence of drug-resistant cells. For example, deep sequencing of paired diagnosis and relapse acute myeloid leukaemia samples has provided direct evidence that relapse in some cases is generated from minor genetic subclones present at diagnosis that survive chemotherapy, suggesting that resistant cells are generated by evolutionary processes before treatment and are selected by therapy. Nevertheless, the mechanisms of therapy failure and capacity for leukaemic regeneration remain obscure, as sequence analysis alone does not provide insight into the cell types that are fated to drive relapse. Although leukaemia stem cells have been linked to relapse owing to their dormancy and self-renewal properties, and leukaemia stem cell gene expression signatures are highly predictive of therapy failure, experimental studies have been primarily correlative and a role for leukaemia stem cells in acute myeloid leukaemia relapse has not been directly proved. Here, through combined genetic and functional analysis of purified subpopulations and xenografts from paired diagnosis/relapse samples, we identify therapy-resistant cells already present at diagnosis and two major patterns of relapse. In some cases, relapse originated from rare leukaemia stem cells with a haematopoietic stem/progenitor cell phenotype, while in other instances relapse developed from larger subclones of immunophenotypically committed leukaemia cells that retained strong stemness transcriptional signatures. The identification of distinct patterns of relapse should lead to improved methods for disease management and monitoring in acute myeloid leukaemia. Moreover, the shared functional and transcriptional stemness properties that underlie both cellular origins of relapse emphasize the importance of developing new therapeutic approaches that target stemness to prevent relapse.
[Mh] Termos MeSH primário: Linhagem da Célula
Leucemia Mieloide Aguda/patologia
Recidiva Local de Neoplasia/patologia
Células-Tronco Neoplásicas/patologia
[Mh] Termos MeSH secundário: Animais
Células Clonais/metabolismo
Células Clonais/patologia
Feminino
Seres Humanos
Imunofenotipagem
Leucemia Mieloide Aguda/genética
Camundongos
Mutação
Células Progenitoras Mieloides/metabolismo
Células Progenitoras Mieloides/patologia
Recidiva Local de Neoplasia/genética
Células-Tronco Neoplásicas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[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:170629
[St] Status:MEDLINE
[do] DOI:10.1038/nature22993


  6 / 912 MEDLINE  
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[PMID]:28436985
[Au] Autor:Vu LP; Prieto C; Amin EM; Chhangawala S; Krivtsov A; Calvo-Vidal MN; Chou T; Chow A; Minuesa G; Park SM; Barlowe TS; Taggart J; Tivnan P; Deering RP; Chu LP; Kwon JA; Meydan C; Perales-Paton J; Arshi A; Gönen M; Famulare C; Patel M; Paietta E; Tallman MS; Lu Y; Glass J; Garret-Bakelman FE; Melnick A; Levine R; Al-Shahrour F; Järås M; Hacohen N; Hwang A; Garippa R; Lengner CJ; Armstrong SA; Cerchietti L; Cowley GS; Root D; Doench J; Leslie C; Ebert BL; Kharas MG
[Ad] Endereço:Molecular Pharmacology Program, Center for Cell Engineering, Center for Stem Cell Biology, and Center for Experimental Therapeutics, Memorial Sloan Kettering Cancer Center, New York, New York, USA.
[Ti] Título:Functional screen of MSI2 interactors identifies an essential role for SYNCRIP in myeloid leukemia stem cells.
[So] Source:Nat Genet;49(6):866-875, 2017 Jun.
[Is] ISSN:1546-1718
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The identity of the RNA-binding proteins (RBPs) that govern cancer stem cells remains poorly characterized. The MSI2 RBP is a central regulator of translation of cancer stem cell programs. Through proteomic analysis of the MSI2-interacting RBP network and functional shRNA screening, we identified 24 genes required for in vivo leukemia. Syncrip was the most differentially required gene between normal and myeloid leukemia cells. SYNCRIP depletion increased apoptosis and differentiation while delaying leukemogenesis. Gene expression profiling of SYNCRIP-depleted cells demonstrated a loss of the MLL and HOXA9 leukemia stem cell program. SYNCRIP and MSI2 interact indirectly though shared mRNA targets. SYNCRIP maintains HOXA9 translation, and MSI2 or HOXA9 overexpression rescued the effects of SYNCRIP depletion. Altogether, our data identify SYNCRIP as a new RBP that controls the myeloid leukemia stem cell program. We propose that targeting these RBP complexes might provide a novel therapeutic strategy in leukemia.
[Mh] Termos MeSH primário: Regulação Leucêmica da Expressão Gênica
Ribonucleoproteínas Nucleares Heterogêneas/genética
Leucemia Mieloide/genética
Proteínas de Ligação a RNA/metabolismo
[Mh] Termos MeSH secundário: Animais
Sobrevivência Celular
Feminino
Hematopoese/genética
Ribonucleoproteínas Nucleares Heterogêneas/metabolismo
Proteínas de Homeodomínio/genética
Seres Humanos
Leucemia Aguda Bifenotípica/genética
Leucemia Aguda Bifenotípica/patologia
Leucemia Mieloide/patologia
Camundongos Endogâmicos C57BL
Camundongos Knockout
Células Progenitoras Mieloides/metabolismo
Células Progenitoras Mieloides/patologia
RNA Interferente Pequeno
Proteínas de Ligação a RNA/genética
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Heterogeneous-Nuclear Ribonucleoproteins); 0 (Homeodomain Proteins); 0 (MSI2 protein, human); 0 (RNA, Small Interfering); 0 (RNA-Binding Proteins); 0 (SYNCRIP protein, human); 0 (Syncrip protein, mouse); 0 (homeobox protein HOXA9)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170425
[St] Status:MEDLINE
[do] DOI:10.1038/ng.3854


  7 / 912 MEDLINE  
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[PMID]:28432220
[Au] Autor:Wallace JA; Kagele DA; Eiring AM; Kim CN; Hu R; Runtsch MC; Alexander M; Huffaker TB; Lee SH; Patel AB; Mosbruger TL; Voth WP; Rao DS; Miles RR; Round JL; Deininger MW; O'Connell RM
[Ad] Endereço:Department of Pathology and.
[Ti] Título:miR-155 promotes FLT3-ITD-induced myeloproliferative disease through inhibition of the interferon response.
[So] Source:Blood;129(23):3074-3086, 2017 Jun 08.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:FLT3-ITD acute myeloid leukemia (AML) accounts for ∼25% of all AML cases and is a subtype that carries a poor prognosis. microRNA-155 (miR-155) is specifically overexpressed in FLT3-ITD AML compared with FLT3 wild-type (FLT3-WT) AML and is critical for the growth of FLT3-ITD AML cells in vitro. However, miR-155's role in regulating FLT3-ITD-mediated disease in vivo remains unclear. In this study, we used a genetic mouse model to determine whether miR-155 influences the development of FLT3-ITD-induced myeloproliferative disease. Results indicate that miR-155 promotes FLT3-ITD-induced myeloid expansion in the bone marrow, spleen, and peripheral blood. Mechanistically, miR-155 increases proliferation of the hematopoietic stem and progenitor cell compartments by reducing the growth-inhibitory effects of the interferon (IFN) response, and this involves targeting of Cebpb. Consistent with our observations in mice, primary FLT3-ITD AML clinical samples have significantly higher miR-155 levels and a lower IFN response compared with FLT3-WT AML samples. Further, inhibition of miR-155 in FLT3-ITD AML cell lines using CRISPR/Cas9, or primary FLT3-ITD AML samples using locked nucleic acid antisense inhibitors, results in an elevated IFN response and reduces colony formation. Altogether, our data reveal that miR-155 collaborates with FLT3-ITD to promote myeloid cell expansion in vivo and that this involves a multitarget mechanism that includes repression of IFN signaling.
[Mh] Termos MeSH primário: Interferons/biossíntese
MicroRNAs/genética
Transtornos Mieloproliferativos/etiologia
Tirosina Quinase 3 Semelhante a fms/genética
[Mh] Termos MeSH secundário: Animais
Sistemas CRISPR-Cas
Linhagem Celular Tumoral
Modelos Animais de Doenças
Feminino
Seres Humanos
Leucemia Mieloide Aguda/etiologia
Leucemia Mieloide Aguda/genética
Leucemia Mieloide Aguda/imunologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Camundongos Mutantes
MicroRNAs/antagonistas & inibidores
Mutação
Células Progenitoras Mieloides/imunologia
Células Progenitoras Mieloides/patologia
Mielopoese/genética
Transtornos Mieloproliferativos/genética
Transtornos Mieloproliferativos/imunologia
Ensaio Tumoral de Célula-Tronco
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MIRN155 microRNA, human); 0 (MicroRNAs); 0 (Mirn155 microRNA, mouse); 9008-11-1 (Interferons); EC 2.7.10.1 (FLT3 protein, human); EC 2.7.10.1 (Flt3 protein, mouse); EC 2.7.10.1 (fms-Like Tyrosine Kinase 3)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170913
[Lr] Data última revisão:
170913
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170423
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2016-09-740209


  8 / 912 MEDLINE  
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[PMID]:28248934
[Au] Autor:Kingwell K
[Ti] Título:Cancer: CD99 marks malignant myeloid stem cells.
[So] Source:Nat Rev Drug Discov;16(3):166, 2017 03 01.
[Is] ISSN:1474-1784
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Moléculas de Adesão Celular
Neoplasias
[Mh] Termos MeSH secundário: Antígenos CD
Seres Humanos
Células Progenitoras Mieloides
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Cell Adhesion Molecules)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171026
[Lr] Data última revisão:
171026
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170302
[St] Status:MEDLINE
[do] DOI:10.1038/nrd.2017.31


  9 / 912 MEDLINE  
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[PMID]:28087538
[Au] Autor:Duggan JM; Buechler MB; Olson RM; Hohl TM; Hamerman JA
[Ad] Endereço:Immunology Program, Benaroya Research Institute, Seattle, WA.
[Ti] Título:BCAP inhibits proliferation and differentiation of myeloid progenitors in the steady state and during demand situations.
[So] Source:Blood;129(11):1503-1513, 2017 Mar 16.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:B-cell adaptor for phosphatidylinositol 3-kinase (BCAP) is a signaling adaptor expressed in mature hematopoietic cells, including monocytes and neutrophils. Here we investigated the role of BCAP in the homeostasis and development of these myeloid lineages. BCAP mice had more bone marrow (BM) monocytes than wild-type (WT) mice, and in mixed WT:BCAP BM chimeras, monocytes and neutrophils skewed toward BCAP origin, showing a competitive advantage for BCAP myeloid cells. BCAP was expressed in BM hematopoietic progenitors, including lineage Sca-1 c-kit (LSK), common myeloid progenitor, and granulocyte/macrophage progenitor (GMP) cells. At the steady state, BCAP GMP cells expressed more IRF8 and less C/EBPα than did WT GMP cells, which correlated with an increase in monocyte progenitors and a decrease in granulocyte progenitors among GMP cells. Strikingly, BCAP progenitors proliferated and produced more myeloid cells of both neutrophil and monocyte/macrophage lineages than did WT progenitors in myeloid colony-forming unit assays, supporting a cell-intrinsic role of BCAP in inhibiting myeloid proliferation and differentiation. Consistent with these findings, during cyclophosphamide-induced myeloablation or specific monocyte depletion, BCAP mice replenished circulating monocytes and neutrophils earlier than WT mice. During myeloid replenishment after cyclophosphamide-induced myeloablation, BCAP mice had increased LSK proliferation and increased numbers of LSK and GMP cells compared with WT mice. Furthermore, BCAP mice accumulated more monocytes and neutrophils in the spleen than did WT mice during infection. Together, these data identify BCAP as a novel inhibitor of myelopoiesis in the steady state and of emergency myelopoiesis during demand conditions.
[Mh] Termos MeSH primário: Proteínas Adaptadoras de Transdução de Sinal/fisiologia
Diferenciação Celular
Proliferação Celular
Células Progenitoras Mieloides/citologia
[Mh] Termos MeSH secundário: Animais
Linhagem da Célula
Homeostase
Camundongos
Monócitos/citologia
Mielopoese
Neutrófilos/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (Pik3ap1 protein, mouse)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170823
[Lr] Data última revisão:
170823
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170115
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2016-06-719823


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[PMID]:27940198
[Au] Autor:Ciapetti G; Di Pompo G; Avnet S; Martini D; Diez-Escudero A; Montufar EB; Ginebra MP; Baldini N
[Ad] Endereço:Orthopaedic Pathophysiology and Regenerative Medicine Unit, Istituto Ortopedico Rizzoli, Bologna, Italy. Electronic address: gabriela.ciapetti@ior.it.
[Ti] Título:Osteoclast differentiation from human blood precursors on biomimetic calcium-phosphate substrates.
[So] Source:Acta Biomater;50:102-113, 2017 Mar 01.
[Is] ISSN:1878-7568
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The design of synthetic bone grafts to foster bone formation is a challenge in regenerative medicine. Understanding the interaction of bone substitutes with osteoclasts is essential, since osteoclasts not only drive a timely resorption of the biomaterial, but also trigger osteoblast activity. In this study, the adhesion and differentiation of human blood-derived osteoclast precursors (OCP) on two different micro-nanostructured biomimetic hydroxyapatite materials consisting in coarse (HA-C) and fine HA (HA-F) crystals, in comparison with sintered stoichiometric HA (sin-HA, reference material), were investigated. Osteoclasts were induced to differentiate by RANKL-containing supernatant using cell/substrate direct and indirect contact systems, and calcium (Ca ) and phosphorus (P ) in culture medium were measured. We observed that OCP adhered to the experimental surfaces, and that osteoclast-like cells formed at a rate influenced by the micro- and nano-structure of HA, which also modulate extracellular Ca . Qualitative differences were found between OCP on biomimetic HA-C and HA-F and their counterparts on plastic and sin-HA. On HA-C and HA-F cells shared typical features of mature osteoclasts, i.e. podosomes, multinuclearity, tartrate acid phosphatase (TRAP)-positive staining, and TRAP5b-enzyme release. However, cells were less in number compared to those on plastic or on sin-HA, and they did not express some specific osteoclast markers. In conclusion, blood-derived OCP are able to attach to biomimetic and sintered HA substrates, but their subsequent fusion and resorptive activity are hampered by surface micro-nano-structure. Indirect cultures suggest that fusion of OCP is sensitive to topography and to extracellular calcium. STATEMENT OF SIGNIFICANCE: The novelty of the paper is the differentiation of human blood-derived osteoclast precursors, instead of mouse-derived macrophages as used in most studies, directly on biomimetic micro-nano structured HA-based surfaces, as triggered by osteoblast-produced factors (RANKL/OPG), and influenced by chemistry and topography of the substrate(s). Biomimetic HA-surfaces, like those obtained in calcium phosphate cements, are very different from the conventional calcium phosphate ceramics, both in terms of topography and ion exchange. The role of these factors in modulating precursors' differentiation and activity is analysed. The system is closely reproducing the physiological process of attachment of host cells and further maturation to osteoclasts toward resorption of the substrate, which occurs in vivo after filling bone defects with the calcium phosphate grafts.
[Mh] Termos MeSH primário: Materiais Biomiméticos
Substitutos Ósseos
Diferenciação Celular/efeitos dos fármacos
Durapatita
Células Progenitoras Mieloides/metabolismo
Nanoestruturas/química
Osteoclastos/metabolismo
[Mh] Termos MeSH secundário: Materiais Biomiméticos/química
Materiais Biomiméticos/farmacologia
Substitutos Ósseos/química
Substitutos Ósseos/farmacologia
Adesão Celular/efeitos dos fármacos
Durapatita/química
Durapatita/farmacologia
Seres Humanos
Ligante RANK/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bone Substitutes); 0 (RANK Ligand); 0 (TNFSF11 protein, human); 91D9GV0Z28 (Durapatite)
[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:161213
[St] Status:MEDLINE



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