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[PMID]:29324844
[Au] Autor:Barakat DJ; Suresh R; Barberi T; Pienta KJ; Simons BW; Friedman AD
[Ad] Endereço:Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.
[Ti] Título:Absence of myeloid Klf4 reduces prostate cancer growth with pro-atherosclerotic activation of tumor myeloid cells and infiltration of CD8 T cells.
[So] Source:PLoS One;13(1):e0191188, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The microenvironment of prostate cancer often includes abundant tumor-associated macrophages (TAMs), with their acquisition of an M2 phenotype correlating with local aggressiveness and metastasis. Tumor-derived M-CSF contributes to TAM M2 polarization, and M-CSF receptor inhibition slows prostate cancer growth in model systems. As additional cytokines can direct TAM M2 polarization, targeting downstream transcription factors could avoid resistance. Klf4 and C/EBPß each contribute to monocyte development, and reduced expression of macrophage Klf4 or C/EBPß favors their adoption of a pro-inflammatory M1 state. We find that a Hi-Myc C57BL/6 prostate cancer line grows more slowly in syngeneic Klf4(f/f);Lys-Cre compared with Klf4(f/f) mice when inoculated subcutaneously, but grows equally rapidly in C/EBPß(f/f);Lys-Cre and C/EBPß(f/f) hosts. In the absence of myeloid Klf4, TAMs have reduced expression of surface mannose receptor and Fizz1 mRNA, both M2 markers. Global gene expression analysis further revealed activation of pro-inflammatory, pro-atherosclerotic pathways. Analysis of tumor-infiltrating lymphocytes (TILs) demonstrated markedly increased activated CD8 T cell numbers, and CD8 T cell depletion obviated the inhibitory effect of myeloid Klf4 deletion on prostate cancer growth. These findings suggest that reducing expression or activity of the Klf4 transcription factor in tumor myeloid cells may contribute to prostate cancer therapy.
[Mh] Termos MeSH primário: Fatores de Transcrição Kruppel-Like/deficiência
Neoplasias da Próstata/metabolismo
Neoplasias da Próstata/patologia
[Mh] Termos MeSH secundário: Animais
Aterosclerose/etiologia
Proteína beta Intensificadora de Ligação a CCAAT/deficiência
Proteína beta Intensificadora de Ligação a CCAAT/genética
Antígeno CD11c/metabolismo
Linfócitos T CD8-Positivos/imunologia
Linfócitos T CD8-Positivos/patologia
Linhagem Celular Tumoral
Fatores de Transcrição Kruppel-Like/genética
Lectinas Tipo C/metabolismo
Linfócitos do Interstício Tumoral
Macrófagos/imunologia
Macrófagos/metabolismo
Macrófagos/patologia
Masculino
Lectinas de Ligação a Manose/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Células Mieloides/imunologia
Células Mieloides/metabolismo
Células Mieloides/patologia
Neoplasias da Próstata/genética
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
RNA Neoplásico/genética
RNA Neoplásico/metabolismo
Receptores de Superfície Celular/metabolismo
Microambiente Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (CCAAT-Enhancer-Binding Protein-beta); 0 (CD11c Antigen); 0 (GKLF protein); 0 (Kruppel-Like Transcription Factors); 0 (Lectins, C-Type); 0 (Mannose-Binding Lectins); 0 (RNA, Messenger); 0 (RNA, Neoplasm); 0 (Receptors, Cell Surface); 0 (mannose receptor)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180112
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191188


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[PMID]:28657144
[Au] Autor:Yu HF; Tao R; Yang ZQ; Wang K; Yue ZP; Guo B
[Ad] Endereço:College of Veterinary Medicine, Jilin University, Changchun, P.R. China.
[Ti] Título:Ptn functions downstream of C/EBPß to mediate the effects of cAMP on uterine stromal cell differentiation through targeting Hand2 in response to progesterone.
[So] Source:J Cell Physiol;233(2):1612-1626, 2018 Feb.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ptn is a pleiotropic growth factor involving in the regulation of cellular proliferation and differentiation, but its biological function in uterine decidualization remains unknown. Here, we showed that Ptn was highly expressed in the decidual cells, and could induce the proliferation of uterine stromal cells and expression of Prl8a2 and Prl3c1 which were two well-established differentiation markers for decidualization, suggesting an important role of Ptn in decidualization. In the uterine stromal cells, progesterone stimulated the expression of Ptn accompanied with an accumulation of intracellular cAMP level. Silencing of Ptn impeded the induction of progesterone and cAMP on the differentiation of uterine stromal cells. Administration of PKA inhibitor H89 resulted in a blockage of progesterone on Ptn expression. Further analysis evidenced that regulation of progesterone and cAMP on Ptn was mediated by C/EBPß. During in vitro decidualization, knockdown of Ptn could weaken the up-regulation of Prl8a2 and Prl3c1 elicited by C/EBPß overexpression, while constitutive activation of Ptn reversed the repressive effects of C/EBPß siRNA on the expression of Prl8a2 and Prl3c1. Meanwhile, Ptn might mediate the regulation of C/EBPß on Hand2 which was a downstream target of Ptn in the differentiation of uterine stromal cells. Attenuation of Ptn or C/EBPß by specific siRNA blocked the stimulation of Hand2 by progesterone and cAMP. Collectively, Ptn may play a vital role in the progesterone-induced decidualization pathway.
[Mh] Termos MeSH primário: 8-Bromo Monofosfato de Adenosina Cíclica/farmacologia
Fatores de Transcrição Hélice-Alça-Hélice Básicos/metabolismo
Proteína beta Intensificadora de Ligação a CCAAT/metabolismo
Proteínas de Transporte/metabolismo
Diferenciação Celular/efeitos dos fármacos
Citocinas/metabolismo
Decídua/efeitos dos fármacos
Progesterona/farmacologia
Células Estromais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Fatores de Transcrição Hélice-Alça-Hélice Básicos/genética
Proteína beta Intensificadora de Ligação a CCAAT/genética
Proteínas de Transporte/genética
Proliferação Celular/efeitos dos fármacos
Células Cultivadas
Proteínas Quinases Dependentes de AMP Cíclico/metabolismo
Citocinas/genética
Decídua/citologia
Decídua/metabolismo
Feminino
Regulação da Expressão Gênica
Camundongos
Gravidez
Prolactina/análogos & derivados
Prolactina/genética
Prolactina/metabolismo
Interferência de RNA
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Transdução de Sinais/efeitos dos fármacos
Células Estromais/metabolismo
Fatores de Tempo
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Basic Helix-Loop-Helix Transcription Factors); 0 (CCAAT-Enhancer-Binding Protein-beta); 0 (Carrier Proteins); 0 (Cebpb protein, mouse); 0 (Cytokines); 0 (Dtprp protein, mouse); 0 (Hand2 protein, mouse); 0 (RNA, Messenger); 134034-50-7 (pleiotrophin); 23583-48-4 (8-Bromo Cyclic Adenosine Monophosphate); 4G7DS2Q64Y (Progesterone); 9002-62-4 (Prolactin); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170629
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.26067


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[PMID]:28977591
[Au] Autor:Tamura I; Shirafuta Y; Jozaki K; Kajimura T; Shinagawa M; Maekawa R; Taketani T; Asada H; Sato S; Tamura H; Sugino N
[Ad] Endereço:Department of Obstetrics and Gynecology, Yamaguchi University Graduate School of Medicine, Minamikogushi 1-1-1, Ube 755-8505, Japan.
[Ti] Título:Novel Function of a Transcription Factor WT1 in Regulating Decidualization in Human Endometrial Stromal Cells and Its Molecular Mechanism.
[So] Source:Endocrinology;158(10):3696-3707, 2017 Oct 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The Wilms tumor suppressor gene (WT1) encodes an essential transcription factor regulating mammalian urogenital development. However, the function of WT1 in human endometrium is still unclear. The current study examined the involvement of WT1 in the regulation of IGF-binding protein-1 (IGFBP-1) and prolactin (PRL), which are specific markers of decidualization, in human endometrial stromal cells (ESCs) undergoing decidualization. ESCs isolated from proliferative-phase endometrium were incubated with cyclic adenosine monophosphate (cAMP) to induce decidualization. cAMP increased WT1 expression with the induction of IGFBP-1 and PRL. Knockdown of WT1 by small interfering RNA inhibited cAMP-induced expression of IGFBP-1 and PRL. cAMP also induced the recruitment of WT1 to the IGFBP-1 and PRL promoters. To investigate the mechanism by which WT1 is upregulated by cAMP, we focused on C/EBPß, a gene that regulates the expression of many genes during decidualization. Knockdown of C/EBPß decreased cAMP-increased WT1 expression. cAMP increased the recruitment of C/EBPß to the WT1 enhancer that is located approximately 14,000 bp downstream from the transcription start site. To test the endogenous function of the WT1 enhancer region on WT1 expression, the endogenous WT1 enhancer region was deleted by CRISPR/Cas9 system in HEK293 cells. The increase of WT1 expression by cAMP was not observed in the enhancer-deleted clones. Chromatin immunoprecipitation assay revealed that this enhancer region has high levels of H3K27ac and H3K4me1, which are active enhancer marks. These results show the role of WT1 in regulating decidualization in human ESCs. C/EBPß is an upstream gene that regulates WT1 expression by binding to the novel enhancer region.
[Mh] Termos MeSH primário: Proteína beta Intensificadora de Ligação a CCAAT/genética
AMP Cíclico/metabolismo
Decídua/metabolismo
Proteína 1 de Ligação a Fator de Crescimento Semelhante à Insulina/metabolismo
Prolactina/metabolismo
Células Estromais/metabolismo
Proteínas WT1/genética
[Mh] Termos MeSH secundário: Proteína beta Intensificadora de Ligação a CCAAT/metabolismo
Sistemas CRISPR-Cas
Imunoprecipitação da Cromatina
Decídua/citologia
Endométrio/citologia
Endométrio/metabolismo
Elementos Facilitadores Genéticos
Feminino
Técnicas de Silenciamento de Genes
Células HEK293
Histonas/metabolismo
Seres Humanos
Proteínas WT1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCAAT-Enhancer-Binding Protein-beta); 0 (CEBPB protein, human); 0 (Histones); 0 (IGFBP1 protein, human); 0 (Insulin-Like Growth Factor Binding Protein 1); 0 (WT1 Proteins); 0 (WT1 protein, human); 9002-62-4 (Prolactin); E0399OZS9N (Cyclic AMP)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171005
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-00478


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[PMID]:28938016
[Au] Autor:Wang J; Ma HY; Krishnamoorthy RR; Yorio T; He S
[Ad] Endereço:Department of Ophthalmology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, People's Republic of China.
[Ti] Título:A feed-forward regulation of endothelin receptors by c-Jun in human non-pigmented ciliary epithelial cells and retinal ganglion cells.
[So] Source:PLoS One;12(9):e0185390, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:c-Jun, c-Jun N-terminal kinase(JNK) and endothelin B (ETB) receptor have been shown to contribute to the pathogenesis of glaucoma. Previously, we reported that an increase of c-Jun and CCAAT/enhancer binding protein ß (C/EBPß) immunohistostaining is associated with upregulation of the ETB receptor within the ganglion cell layer of rats with elevated intraocular pressure (IOP). In addition, both transcription factors regulate the expression of the ETB receptor in human non-pigmented ciliary epithelial cells (HNPE). The current study addressed the mechanisms by which ET-1 produced upregulation of ET receptors in primary rat retinal ganglion cells (RGCs) and HNPE cells. Treatment of ET-1 and ET-3 increased the immunocytochemical staining of c-Jun and C/EBPß in primary rat RGCs and co-localization of both transcription factors was observed. A marked increase in DNA binding activity of AP-1 and C/EBPß as well as elevated protein levels of c-Jun and c-Jun-N-terminal kinase (JNK) were detected following ET-1 treatment in HNPE cells. Overexpression of ETA or ETB receptor promoted the upregulation of c-Jun and also elevated its promoter activity. In addition, upregulation of C/EBPß augmented DNA binding and mRNA expression of c-Jun, and furthermore, the interaction of c-Jun and C/EBPß was confirmed using co-immunoprecipitation. Apoptosis of HNPE cells was identified following ET-1 treatment, and overexpression of the ETA or ETB receptor produced enhanced apoptosis. ET-1 mediated upregulation of c-Jun and C/EBPß and their interaction may represent a novel mechanism contributing to the regulation of endothelin receptor expression. Reciprocally, c-Jun was also found to regulate the ET receptors and C/EBPß appeared to play a regulatory role in promoting expression of c-Jun. Taken together, the data suggests that ET-1 triggers the upregulation of c-Jun through both ETA and ETB receptors, and conversely c-Jun also upregulates endothelin receptor expression, thereby generating a positive feed-forward loop of endothelin receptor activation and expression. This feed-forward regulation may contribute to RGC death and astrocyte proliferation following ET-1 treatment.
[Mh] Termos MeSH primário: Células Epiteliais/enzimologia
Proteínas Quinases JNK Ativadas por Mitógeno/metabolismo
Receptores de Endotelina/metabolismo
Células Ganglionares da Retina/enzimologia
[Mh] Termos MeSH secundário: Animais
Apoptose/fisiologia
Proteína beta Intensificadora de Ligação a CCAAT/metabolismo
Células Cultivadas
Cílios/enzimologia
Endotelina-1/metabolismo
Seres Humanos
Ligação Proteica
Ratos Sprague-Dawley
Fator de Transcrição AP-1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCAAT-Enhancer-Binding Protein-beta); 0 (Cebpb protein, rat); 0 (Endothelin-1); 0 (Receptors, Endothelin); 0 (Transcription Factor AP-1); EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170923
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185390


  5 / 1662 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


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[PMID]:28892778
[Au] Autor:Lin PL; Wu TC; Wu DW; Wang L; Chen CY; Lee H
[Ad] Endereço:Graduate Institute of Cancer Biology and Drug Discovery, Taipei Medical University, Taipei, Taiwan.
[Ti] Título:An increase in BAG-1 by PD-L1 confers resistance to tyrosine kinase inhibitor in non-small cell lung cancer via persistent activation of ERK signalling.
[So] Source:Eur J Cancer;85:95-105, 2017 Nov.
[Is] ISSN:1879-0852
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:High programmed cell death 1 ligand 1 (PD-L1) expression in tumour tissues was associated with poor outcomes in non-small cell lung cancer (NSCLC) due to evasion of tumour immune surveillance. However, the role of PD-L1 in tumour invasion and resistance to tyrosine kinase inhibitor (TKI) treatments is not fully understood. Here, we provide evidence to support the involvement of PD-L1 expression in the invasiveness and TKI resistance in NSCLC cells by increased Bcl-2-associated athanogene-1 (BAG-1) expression. The upregulation of BAG-1 transcription by PD-L1 was verified by constructing the BAG-1 promoters using the polymerase chain reaction (PCR) and deletion mutations for luciferase reporter assays. The results indicated that C/EBPß phosphorylation by extracellular signal-regulated kinase (ERK) signalling was responsible for PD-L1-mediated BAG-1 transcription. Mechanistically, the PD-L1-induced BAG-1 expression reciprocally increased PD-L1 expression due to persistent activation of ERK signalling, and it consequently conferred TKI resistance in NSCLC cells. The mechanistic action of this cell model was further confirmed by an animal model, affirming that PD-L1 conferred tumour invasiveness and TKI resistance via persistent activation of ERK signalling by the PD-L1/BAG-1 axis. We therefore suggest a combination of an ERK inhibitor with a TKI as a potential strategy for conquering PD-L1-mediated tumour invasion and TKI resistance in NSCLC patients whose tumours harbour high PD-L1/high BAG-1 expression.
[Mh] Termos MeSH primário: Antígeno B7-H1/metabolismo
Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico
Proteínas de Ligação a DNA/metabolismo
Resistência a Medicamentos Antineoplásicos
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Neoplasias Pulmonares/tratamento farmacológico
Inibidores de Proteínas Quinases/farmacologia
Quinazolinas/farmacologia
Transdução de Sinais/efeitos dos fármacos
Fatores de Transcrição/metabolismo
[Mh] Termos MeSH secundário: Células A549
Animais
Anticorpos Monoclonais/farmacologia
Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia
Antígeno B7-H1/antagonistas & inibidores
Antígeno B7-H1/genética
Proteína 11 Semelhante a Bcl-2/metabolismo
Proteína beta Intensificadora de Ligação a CCAAT/metabolismo
Carcinoma Pulmonar de Células não Pequenas/enzimologia
Carcinoma Pulmonar de Células não Pequenas/genética
Carcinoma Pulmonar de Células não Pequenas/patologia
Movimento Celular/efeitos dos fármacos
Proteínas de Ligação a DNA/genética
Intervalo Livre de Doença
Ativação Enzimática
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Neoplasias Pulmonares/enzimologia
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/patologia
Camundongos Endogâmicos BALB C
Camundongos Nus
Invasividade Neoplásica
Fosforilação
Regiões Promotoras Genéticas
Ligação Proteica
Estabilidade Proteica
Interferência de RNA
Receptor do Fator de Crescimento Epidérmico/antagonistas & inibidores
Receptor do Fator de Crescimento Epidérmico/genética
Receptor do Fator de Crescimento Epidérmico/metabolismo
Fatores de Tempo
Fatores de Transcrição/genética
Transcrição Genética
Transfecção
Regulação para Cima
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (B7-H1 Antigen); 0 (BCL2-associated athanogene 1 protein); 0 (BCL2L11 protein, human); 0 (Bcl-2-Like Protein 11); 0 (CCAAT-Enhancer-Binding Protein-beta); 0 (CD274 protein, human); 0 (CEBPB protein, human); 0 (DNA-Binding Proteins); 0 (Protein Kinase Inhibitors); 0 (Quinazolines); 0 (Transcription Factors); EC 2.7.10.1 (EGFR protein, human); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); S65743JHBS (gefitinib)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170912
[St] Status:MEDLINE


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[PMID]:28854265
[Au] Autor:Fukunaka A; Fukada T; Bhin J; Suzuki L; Tsuzuki T; Takamine Y; Bin BH; Yoshihara T; Ichinoseki-Sekine N; Naito H; Miyatsuka T; Takamiya S; Sasaki T; Inagaki T; Kitamura T; Kajimura S; Watada H; Fujitani Y
[Ad] Endereço:Department of Metabolism & Endocrinology, Juntendo University Graduate School of Medicine, Tokyo, Japan.
[Ti] Título:Zinc transporter ZIP13 suppresses beige adipocyte biogenesis and energy expenditure by regulating C/EBP-ß expression.
[So] Source:PLoS Genet;13(8):e1006950, 2017 Aug.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Given the relevance of beige adipocytes in adult humans, a better understanding of the molecular circuits involved in beige adipocyte biogenesis has provided new insight into human brown adipocyte biology. Genetic mutations in SLC39A13/ZIP13, a member of zinc transporter family, are known to reduce adipose tissue mass in humans; however, the underlying mechanisms remains unknown. Here, we demonstrate that the Zip13-deficient mouse shows enhanced beige adipocyte biogenesis and energy expenditure, and shows ameliorated diet-induced obesity and insulin resistance. Both gain- and loss-of-function studies showed that an accumulation of the CCAAT/enhancer binding protein-ß (C/EBP-ß) protein, which cooperates with dominant transcriptional co-regulator PR domain containing 16 (PRDM16) to determine brown/beige adipocyte lineage, is essential for the enhanced adipocyte browning caused by the loss of ZIP13. Furthermore, ZIP13-mediated zinc transport is a prerequisite for degrading the C/EBP-ß protein to inhibit adipocyte browning. Thus, our data reveal an unexpected association between zinc homeostasis and beige adipocyte biogenesis, which may contribute significantly to the development of new therapies for obesity and metabolic syndrome.
[Mh] Termos MeSH primário: Proteína beta Intensificadora de Ligação a CCAAT/genética
Proteínas de Transporte de Cátions/genética
Proteínas de Ligação a DNA/genética
Obesidade/genética
Fatores de Transcrição/genética
[Mh] Termos MeSH secundário: Adipócitos Bege/metabolismo
Adipogenia/genética
Animais
Proteínas de Transporte de Cátions/metabolismo
Linhagem da Célula
Proteínas de Ligação a DNA/metabolismo
Dieta Hiperlipídica
Metabolismo Energético/genética
Seres Humanos
Resistência à Insulina/genética
Camundongos
Camundongos Knockout
Obesidade/metabolismo
Obesidade/patologia
Fatores de Transcrição/metabolismo
Zinco/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCAAT-Enhancer-Binding Protein-beta); 0 (Cation Transport Proteins); 0 (Cebpb protein, mouse); 0 (DNA-Binding Proteins); 0 (Prdm16 protein, mouse); 0 (Slc39a13 protein, mouse); 0 (Transcription Factors); J41CSQ7QDS (Zinc)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171029
[Lr] Data última revisão:
171029
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170831
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1006950


  8 / 1662 MEDLINE  
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[PMID]:28807982
[Au] Autor:Tamura A; Hirai H; Yokota A; Kamio N; Sato A; Shoji T; Kashiwagi T; Torikoshi Y; Miura Y; Tenen DG; Maekawa T
[Ad] Endereço:Department of Transfusion Medicine and Cell Therapy, Kyoto University Hospital, Kyoto, Japan.
[Ti] Título:C/EBPß is required for survival of Ly6C monocytes.
[So] Source:Blood;130(16):1809-1818, 2017 Oct 19.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The transcription factor CCAAT/enhancer-binding protein ß (C/EBPß) is highly expressed in monocytes/macrophages. However, its roles in monopoiesis are largely unknown. Here, we investigated the roles of C/EBPß in monopoiesis. Further subdivision of monocytes revealed that messenger RNA was highly upregulated in Ly6C monocytes in bone marrow. Accordingly, the number of Ly6C monocytes was significantly reduced in mice. Bone marrow chimera experiments and -Cre-mediated deletion of revealed a cell-intrinsic and monocyte-specific requirement for C/EBPß in monopoiesis. In mice, turnover of Ly6C monocytes was highly accelerated and apoptosis of Ly6C monocytes was increased. Expression of , which encodes a receptor for macrophage colony-stimulating factor, was significantly reduced in Ly6C monocytes of mice. C/EBPß bound to positive regulatory elements of and promoted its transcription. Collectively, these results indicate that C/EBPß is a critical factor for Ly6C monocyte survival, at least in part through upregulation of
[Mh] Termos MeSH primário: Apoptose/genética
Proteína beta Intensificadora de Ligação a CCAAT/fisiologia
Monócitos/fisiologia
[Mh] Termos MeSH secundário: Animais
Antígenos Ly/metabolismo
Proteína beta Intensificadora de Ligação a CCAAT/genética
Células COS
Diferenciação Celular/genética
Sobrevivência Celular/genética
Células Cultivadas
Cercopithecus aethiops
Regulação da Expressão Gênica
Camundongos
Camundongos Knockout
Monócitos/metabolismo
Receptores de Fator Estimulador das Colônias de Granulócitos e Macrófagos/genética
Receptores de Fator Estimulador das Colônias de Granulócitos e Macrófagos/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Ly); 0 (CCAAT-Enhancer-Binding Protein-beta); 0 (Csf1r protein, mouse); 0 (Ly-6C antigen, mouse); 0 (Receptors, Granulocyte-Macrophage Colony-Stimulating Factor)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171104
[Lr] Data última revisão:
171104
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170816
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2017-03-772962


  9 / 1662 MEDLINE  
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[PMID]:28784931
[Au] Autor:Shi X; Lin YP; Gao B; Zhang P
[Ad] Endereço:Department of Integrative Medical Sciences, College of Medicine, Northeast Ohio Medical University, Rootstown, Ohio, USA.
[Ti] Título:Impairment of Hematopoietic Precursor Cell Activation during the Granulopoietic Response to Bacteremia in Mice with Chronic-Plus-Binge Alcohol Administration.
[So] Source:Infect Immun;85(11), 2017 Nov.
[Is] ISSN:1098-5522
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Alcohol abuse impairs immune defense. To study the effect of chronic-plus-binge alcohol exposure on the granulopoietic response, acute alcohol intoxication (intraperitoneal injection of 5 g alcohol/kg body weight) was introduced to mice chronically fed on the Lieber-DeCarli low-fat liquid alcohol diet for 5 weeks. Bacteremia was induced by intravenous injection of Bacteremia caused a remarkable increase in marrow lin c-kit Sca-1 cells. Activation of cell proliferation supported the increase in marrow lin c-kit Sca-1 cells. Alcohol administration inhibited this activation of lin c-kit Sca-1 cells. The bone marrow of pair-fed control mice receiving intraperitoneal saline stored a large number of mature granulocytes expressing a high level of Gr1 (Gr1 cells). The proportion of Gr1 cells and the total number of Gr1 cells were markedly reduced in the bone marrow, along with an increase in the ratio of Gr1 granulocytes in peripheral white blood cells following bacteremia. infection stimulated proliferation of granulopoietic precursor cells, resulting in a marked increase in the ratio of immature Gr1 cells in the bone marrow. Alcohol administration itself triggered marrow release of Gr1 cells, resulting in reduction of the marrow granulocyte reserve with an elevation of granulocytes in the circulation. Alcohol also impaired activation of granulopoietic precursor proliferation following bacteremia. Alcohol disrupted lipopolysaccharide (LPS)-TLR4-ERK1/2-cyclin D1 signaling and inhibited upregulation of Sca-1 and C/EBPß expression by lineage-negative marrow cells in response to bacteremia. These results indicate that chronic-plus-binge alcohol exposure inhibits the granulopoietic response by disrupting key cell signaling for hematopoietic precursor cell activation and commitment to granulocyte lineage development.
[Mh] Termos MeSH primário: Bacteriemia/imunologia
Bebedeira/imunologia
Infecções por Escherichia coli/imunologia
Etanol/farmacologia
Regulação da Expressão Gênica/efeitos dos fármacos
Hematopoese/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Antígenos Ly/genética
Antígenos Ly/imunologia
Bacteriemia/genética
Bacteriemia/patologia
Bebedeira/genética
Bebedeira/patologia
Células da Medula Óssea/efeitos dos fármacos
Células da Medula Óssea/imunologia
Células da Medula Óssea/patologia
Proteína beta Intensificadora de Ligação a CCAAT/genética
Proteína beta Intensificadora de Ligação a CCAAT/imunologia
Ciclina D1/genética
Ciclina D1/imunologia
Modelos Animais de Doenças
Escherichia coli/crescimento & desenvolvimento
Escherichia coli/imunologia
Infecções por Escherichia coli/genética
Infecções por Escherichia coli/patologia
Regulação da Expressão Gênica/imunologia
Granulócitos/efeitos dos fármacos
Granulócitos/imunologia
Granulócitos/patologia
Hematopoese/genética
Hematopoese/imunologia
Masculino
Proteínas de Membrana/genética
Proteínas de Membrana/imunologia
Camundongos
Camundongos Endogâmicos BALB C
Proteína Quinase 1 Ativada por Mitógeno/genética
Proteína Quinase 1 Ativada por Mitógeno/imunologia
Proteína Quinase 3 Ativada por Mitógeno/genética
Proteína Quinase 3 Ativada por Mitógeno/imunologia
Nucleotidiltransferases/deficiência
Nucleotidiltransferases/genética
Nucleotidiltransferases/imunologia
Proteínas Proto-Oncogênicas c-kit/genética
Proteínas Proto-Oncogênicas c-kit/imunologia
Transdução de Sinais/imunologia
Receptor 4 Toll-Like/genética
Receptor 4 Toll-Like/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Ly); 0 (CCAAT-Enhancer-Binding Protein-beta); 0 (Ccnd1 protein, mouse); 0 (Cebpb protein, mouse); 0 (Ly6G antigen, mouse); 0 (Ly6a protein, mouse); 0 (Membrane Proteins); 0 (Tlr4 protein, mouse); 0 (Toll-Like Receptor 4); 136601-57-5 (Cyclin D1); 3K9958V90M (Ethanol); EC 2.7.10.1 (Proto-Oncogene Proteins c-kit); EC 2.7.11.24 (Mapk1 protein, mouse); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3); EC 2.7.7.- (Nucleotidyltransferases); EC 2.7.7.- (lincosaminide O-nucleotidyltransferase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171025
[Lr] Data última revisão:
171025
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170809
[St] Status:MEDLINE


  10 / 1662 MEDLINE  
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[PMID]:28760550
[Au] Autor:Shu S; Xu Y; Xie L; Ouyang Y
[Ad] Endereço:Anesthesiology Department, Children's Hospital of FudanUniversity,Shanghai,201102, China. Electronic address: shiyu_shu@fudan.edu.cn.
[Ti] Título:The role of C/EBPß phosphorylation in modulating membrane phospholipids repairing in LPS-induced human lung/bronchial epithelial cells.
[So] Source:Gene;629:76-85, 2017 Sep 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Acute lung injury/acute respiratory distress syndrome (ALI/ARDS) is a common critical emergency with high mortality in clinical practice. The key mechanism of ALI/ARDS is that the excessive inflammatory response damages the integrity of alveolar and bronchial cell membrane and thus affects their basic function. Phospholipids are the main component of cell membranes. Phospholipase A2 (PLA2), which catalyzes the cleavage of membrane phospholipids, is the most important inflammatory mediator of ALI. However, clara cell secretory protein 1 (CCSP1), an endogenous PLA2 inhibitor can increase the self-defense of membrane phospholipids. Thus, CCSP1 up-regulation and PLA2 inhibition constitutes an effective method for ensuring the stability of membrane phospholipids and for the treatment of ALI/ARDS. In the present study, we developed an in vitro model of ALI via lipopolysaccharide (LPS) stimulation of a human bronchial epithelial cell line, BEAS-2B, and assessed the mRNA and protein levels of CCSP1 and PLA2 in the model cells. The results demonstrated LPS induction inhibited the transcription and protein expression of CCSP1, but only the protein level of membrane associated PLA2 was increased, suggesting that in the in vitro ALI model, abnormally regulated CCSP1 transcription plays a crucial role in the damage of cell membrane. To find out the reason that CCSP1 expression was decreased in the ALI model, we predicted, by means of bioinformatics, putative transcription factors which would bind to CCSP1 promoter, examined their background and expression, and found that a transcription factor, CCAAT/enhancer binding protein ß (C/EBP ß), was correlated with the transcription of CCSP1 in the in vitro ALI model, and its phosphorylation in the model was decreased. CHIP-PCR and luciferase reporter assay revealed that C/EBP ß bound to CCSP1 promoter and facilitated its transcription. Therefore, we conclude that there is a C/EBP ß/CCSP1/PLA2 pathway in the in vitro ALI model. The study of underlying mechanism show that the activity of C/EBP ß depends on its phosphorylation:LPS stimulation reduced C/EBP ß phosphorylation and suppressed the transcription of CCSP1 in BEAS-2B cells, which resulted in enhanced PLA2 and the consequent membrane damage. And further study shows that overexpression of CDK2(Cyclindependent kinase 2), promoted the phosphorylation of C/EBP ß and inhibited PLA2 through the C/EBP ß/CCSP1/PLA2 pathway, so as to attenuate membrane damage. The significance of this study lies in that artificial C/EBP ß phosphorylation regulation may ease the membrane damage in ALI and improve membrane repair.
[Mh] Termos MeSH primário: Lesão Pulmonar Aguda/metabolismo
Proteína beta Intensificadora de Ligação a CCAAT/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular
Células Epiteliais/metabolismo
Seres Humanos
Lipopolissacarídeos/metabolismo
Pulmão/citologia
Pulmão/metabolismo
Fosfolipases A2/metabolismo
Fosfolipídeos/metabolismo
Fosforilação
Regiões Promotoras Genéticas
Uteroglobina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCAAT-Enhancer-Binding Protein-beta); 0 (CEBPB protein, human); 0 (Lipopolysaccharides); 0 (Phospholipids); 0 (SCGB1A1 protein, human); 9060-09-7 (Uteroglobin); EC 3.1.1.4 (Phospholipases A2)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170828
[Lr] Data última revisão:
170828
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170802
[St] Status:MEDLINE



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