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[PMID]:29227599
[Au] Autor:Minchenko OH; Kryvdiuk IV; Riabovol OO; Minchenko DO; Danilovskyi SV; Ratushna OO
[Ti] Título:Inhibition of IRE1 modifies the hypoxic regulation of GADD family gene expressions in U87 glioma cells.
[So] Source:Ukr Biochem J;88(2):25-34, 2016 Mar-Apr.
[Is] ISSN:2409-4943
[Cp] País de publicação:Ukraine
[La] Idioma:eng
[Ab] Resumo:We have studied hypoxic regulation of the expression of genes encoded GADD (growth arrest and DNA damage) family proteins in U87 glioma cells in relation to inhibition of IRE1 (inositol requiring enzyme-1), which controls cell proliferation and tumor growth as a central mediator of endoplasmic reticulum stress. We have shown that hypoxia up-regulates the expression of GADD34, GADD45A, GADD45B, and GADD153 genes, which are related to cell proliferation and apoptosis, in control (transfected by empty vector) glioma cells in gene specific manner. At the same time, the expression level of EIF2AK 1 (eukaryotic translation initiation factor 2-alpha kinase 1) and AI FM1 (apoptosis inducing factor, mitochondria associated 1) genes in these cells is down-regulated upon hypoxic condition. It was also shown that inhibition of ІRE1 signaling enzyme function in U87 glioma cells enhances the effect of hypoxia on these genes expression, except EIF2AK 1 and AI FM1 genes. Furthermore, the expression of all studied genes in ІRE1 knockdown cells is significantly decreased upon normoxic condition, except GADD45B gene, which expression level is strongly up-regulated. Therefore, the expression level of genes encoding GADD34, GADD45A, GADD45B, GADD153, EIF2AK 1, and AI FM1 is affected by hypoxia and by inhibition of IRE1-mediated endoplasmic reticulum stress signaling in gene specific manner and correlates with suppression of glioma cell proliferation upon inhibition of the IRE1 enzyme function.
[Mh] Termos MeSH primário: Proteínas de Ciclo Celular/genética
Estresse do Retículo Endoplasmático/genética
Endorribonucleases/genética
Regulação Neoplásica da Expressão Gênica
Neuroglia/metabolismo
Proteínas Nucleares/genética
Proteína Fosfatase 1/genética
Proteínas Serina-Treonina Quinases/genética
[Mh] Termos MeSH secundário: Antígenos de Diferenciação/genética
Antígenos de Diferenciação/metabolismo
Apoptose/genética
Fator de Indução de Apoptose/genética
Fator de Indução de Apoptose/metabolismo
Proteínas de Ciclo Celular/metabolismo
Hipóxia Celular
Linhagem Celular Tumoral
Proliferação Celular
Endorribonucleases/deficiência
Técnicas de Silenciamento de Genes
Seres Humanos
Neuroglia/patologia
Proteínas Nucleares/metabolismo
Plasmídeos/química
Plasmídeos/metabolismo
Proteína Fosfatase 1/metabolismo
Proteínas Serina-Treonina Quinases/deficiência
Transdução de Sinais
Fator de Transcrição CHOP/genética
Fator de Transcrição CHOP/metabolismo
Transfecção
eIF-2 Quinase/genética
eIF-2 Quinase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AIFM1 protein, human); 0 (Antigens, Differentiation); 0 (Apoptosis Inducing Factor); 0 (Cell Cycle Proteins); 0 (DDIT3 protein, human); 0 (GADD45A protein, human); 0 (GADD45B protein, human); 0 (Nuclear Proteins); 147336-12-7 (Transcription Factor CHOP); EC 2.7.11.1 (EIF2AK1 protein, human); EC 2.7.11.1 (ERN1 protein, human); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.1 (eIF-2 Kinase); EC 3.1.- (Endoribonucleases); EC 3.1.3.16 (PPP1R15A protein, human); EC 3.1.3.16 (Protein Phosphatase 1)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE
[do] DOI:10.15407/ubj88.02.025


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[PMID]:27777239
[Au] Autor:Gao X; Lee HY; da Rocha EL; Zhang C; Lu YF; Li D; Feng Y; Ezike J; Elmes RR; Barrasa MI; Cahan P; Li H; Daley GQ; Lodish HF
[Ad] Endereço:Whitehead Institute for Biomedical Research, Cambridge, MA.
[Ti] Título:TGF-ß inhibitors stimulate red blood cell production by enhancing self-renewal of BFU-E erythroid progenitors.
[So] Source:Blood;128(23):2637-2641, 2016 12 08.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Burst-forming unit erythroid progenitors (BFU-Es) are so named based on their ability to generate in methylcellulose culture large colonies of erythroid cells that consist of "bursts" of smaller erythroid colonies derived from the later colony-forming unit erythroid progenitor erythropoietin (Epo)-dependent progenitors. "Early" BFU-E cells forming large BFU-E colonies presumably have higher capacities for self-renewal than do "late" BFU-Es forming small colonies, but the mechanism underlying this heterogeneity remains unknown. We show that the type III transforming growth factor ß (TGF-ß) receptor (TßRIII) is a marker that distinguishes early and late BFU-Es. Transient elevation of TßRIII expression promotes TGF-ß signaling during the early BFU-E to late BFU-E transition. Blocking TGF-ß signaling using a receptor kinase inhibitor increases early BFU-E cell self-renewal and total erythroblast production, suggesting the usefulness of this type of drug in treating Epo-unresponsive anemias.
[Mh] Termos MeSH primário: Antígenos de Diferenciação/metabolismo
Eritrócitos/metabolismo
Células Precursoras Eritroides/metabolismo
Proteoglicanas/metabolismo
Receptores de Fatores de Crescimento Transformadores beta/metabolismo
Transdução de Sinais/fisiologia
Fator de Crescimento Transformador beta/metabolismo
[Mh] Termos MeSH secundário: Anemia/metabolismo
Anemia/terapia
Animais
Eritrócitos/citologia
Células Precursoras Eritroides/citologia
Eritropoetina/metabolismo
Seres Humanos
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, Differentiation); 0 (Proteoglycans); 0 (Receptors, Transforming Growth Factor beta); 0 (Transforming Growth Factor beta); 11096-26-7 (Erythropoietin); 145170-29-2 (betaglycan)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180111
[Lr] Data última revisão:
180111
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE


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[PMID]:29221729
[Au] Autor:Alcántara-Hernández M; Leylek R; Wagar LE; Engleman EG; Keler T; Marinkovich MP; Davis MM; Nolan GP; Idoyaga J
[Ad] Endereço:Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA; Program in Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.
[Ti] Título:High-Dimensional Phenotypic Mapping of Human Dendritic Cells Reveals Interindividual Variation and Tissue Specialization.
[So] Source:Immunity;47(6):1037-1050.e6, 2017 Dec 19.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Given the limited efficacy of clinical approaches that rely on ex vivo generated dendritic cells (DCs), it is imperative to design strategies that harness specialized DC subsets in situ. This requires delineating the expression of surface markers by DC subsets among individuals and tissues. Here, we performed a multiparametric phenotypic characterization and unbiased analysis of human DC subsets in blood, tonsil, spleen, and skin. We uncovered previously unreported phenotypic heterogeneity of human cDC2s among individuals, including variable expression of functional receptors such as CD172a. We found marked differences in DC subsets localized in blood and lymphoid tissues versus skin, and a striking absence of the newly discovered Axl DCs in the skin. Finally, we evaluated the capacity of anti-receptor monoclonal antibodies to deliver vaccine components to skin DC subsets. These results offer a promising path for developing DC subset-specific immunotherapies that cannot be provided by transcriptomic analysis alone.
[Mh] Termos MeSH primário: Antígenos de Diferenciação/imunologia
Variação Biológica Individual
Células Dendríticas/imunologia
Fenótipo
Proteínas Proto-Oncogênicas/imunologia
Receptores Proteína Tirosina Quinases/imunologia
Receptores Imunológicos/imunologia
Pele/imunologia
[Mh] Termos MeSH secundário: Animais
Anticorpos Monoclonais/química
Anticorpos Monoclonais/metabolismo
Anticorpos Monoclonais/farmacocinética
Antígenos CD/genética
Antígenos CD/imunologia
Antígenos de Diferenciação/genética
Biomarcadores/análise
Vacinas Anticâncer/administração & dosagem
Vacinas Anticâncer/biossíntese
Citofotometria/métodos
Células Dendríticas/citologia
Feminino
Expressão Gênica
Seres Humanos
Imunofenotipagem
Imunoterapia
Linfonodos/citologia
Linfonodos/imunologia
Camundongos
Camundongos Endogâmicos C57BL
Terapia de Alvo Molecular
Neoplasias/genética
Neoplasias/imunologia
Neoplasias/patologia
Neoplasias/terapia
Especificidade de Órgãos
Tonsila Palatina/citologia
Tonsila Palatina/imunologia
Proteínas Proto-Oncogênicas/deficiência
Proteínas Proto-Oncogênicas/genética
Receptores Proteína Tirosina Quinases/deficiência
Receptores Proteína Tirosina Quinases/genética
Receptores Imunológicos/genética
Pele/citologia
Baço/citologia
Baço/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Antigens, CD); 0 (Antigens, Differentiation); 0 (Biomarkers); 0 (Cancer Vaccines); 0 (Proto-Oncogene Proteins); 0 (Receptors, Immunologic); 0 (SIRPA protein, human); EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases); EC 2.7.10.1 (axl receptor tyrosine kinase)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171210
[St] Status:MEDLINE


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[PMID]:27776738
[Au] Autor:Cheng Z; Peng HL; Zhang R; Fu XM; Zhang GS
[Ad] Endereço:Department of Hematology, Institute of Molecular Hematology, The Second Xiang-ya Hospital, Central South University, Changsha, Hunan, PR China.
[Ti] Título:Bone marrow-derived innate macrophages attenuate oxazolone-induced colitis.
[So] Source:Cell Immunol;311:46-53, 2017 Jan.
[Is] ISSN:1090-2163
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Previous studies have shown that a subpopulation of granulocyte macrophage colony-stimulating factor (GM-CSF)-dependent F4/80 CD11b innate macrophages could be derived from bone marrow cells by continuous in vitro culturing. These cells could be induced to differentiate into M1 or M2 macrophages in vitro. In the current study, we sought to determine whether bone marrow cell-derived innate macrophages (BMIMs) could be used to fulfill an anti-inflammatory purpose by intravenous transplantation in vivo after being stimulated to differentiate into M2 macrophages. Because Th2 cytokines, such as interleukin IL-4 and IL-13, can induce macrophage polarization into M2 macrophages, we treated the BMIMs with IL-4 and IL-13 in vitro. Next, the M2 macrophages were intravenously transplanted into a typical Th2-mediated inflammatory disease model, oxazolone (OXZ)-induced colitis, to assess the anti-inflammatory activity of BMIM-derived M2 macrophages (BMIM-M2Ms) in vivo. After transplantation, the severity of intestinal inflammation was attenuated. In addition, colon lengths and mouse body weights were noticeably improved. F4/80 CD206 double-positive cells (displaying the markers of M2 macrophages) had accumulated in the colon tissue of BMIM-M2M-transplanted mice. This evidence demonstrated that bone marrow-derived BMIM-M2Ms could be used to alleviate OXZ-induced Th2-mediated inflammation in a mouse model in vivo.
[Mh] Termos MeSH primário: Colite/imunologia
Colite/terapia
Macrófagos/transplante
[Mh] Termos MeSH secundário: Animais
Antígenos de Diferenciação/metabolismo
Antígeno CD11b/metabolismo
Células Cultivadas
Colite/induzido quimicamente
Citocinas/metabolismo
Modelos Animais de Doenças
Fator Estimulador de Colônias de Granulócitos e Macrófagos/metabolismo
Seres Humanos
Imunidade Inata
Lectinas Tipo C/metabolismo
Macrófagos/imunologia
Lectinas de Ligação a Manose/metabolismo
Camundongos
Camundongos Endogâmicos BALB C
Oxazolona
Fenótipo
Receptores de Superfície Celular/metabolismo
Células Th2/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Differentiation); 0 (CD11b Antigen); 0 (Cytokines); 0 (Lectins, C-Type); 0 (Mannose-Binding Lectins); 0 (Receptors, Cell Surface); 0 (mannose receptor); 0 (monocyte-macrophage differentiation antigen); 15646-46-5 (Oxazolone); 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171217
[Lr] Data última revisão:
171217
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE


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[PMID]:29045468
[Au] Autor:Hwang IH; Oh SY; Jang HJ; Jo E; Joo JC; Lee KB; Yoo HS; Lee MY; Park SJ; Jang IS
[Ad] Endereço:Department of Physiology, Korea University College of Medicine, Seoul, Republic of Korea.
[Ti] Título:Cordycepin promotes apoptosis in renal carcinoma cells by activating the MKK7-JNK signaling pathway through inhibition of c-FLIPL expression.
[So] Source:PLoS One;12(10):e0186489, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cellular FLICE inhibitory protein (c-FLIP) is a key anti-apoptotic regulator that associates with the signaling complex downstream of NF-κB, negatively interfering with apoptotic signaling. The role of c-FLIP downregulation by negative regulation of NF-κB signaling during apoptosis is poorly understood. Here, we demonstrate that NF-κB-mediated c-FLIPL negatively regulates the JNK signaling pathway, and that cordycepin treatment of human renal cancer cells leads to apoptosis induction through c-FLIPL inhibition. TNF-α-induced inflammatory microenvironments stimulated NF-κB signaling and the c-FLIP long form (c-FLIPL) in TK-10 cells. Specifically, cordycepin inhibited TNF-α-mediated NF-κB activation, which induced renal cancer cell apoptosis. Cordycepin downregulated GADD45B and c-FLIPL, but upregulated MKK7 and phospho-JNK, by preventing nuclear mobilization of NF-κB. Furthermore, siRNA-mediated knockdown of GADD45B in cordycepin-treated TK-10 cells considerably increased MKK7 compared to cordycepin alone. siRNA-mediated knockdown of c-FLIPL prevented TNF-α-induced JNK inactivation, whereas c-FLIPL overexpression inhibited cordycepin-mediated JNK activation. The JNK inhibitor SP600125 strongly inhibited Bax expression. In nude mice, cordycepin significantly decreased tumor volume. Taken together, the results indicate that cordycepin inhibits TNF-α-mediated NF-κB/GADD45B signaling, which activates the MKK7-JNK signaling pathway through inhibition of c-FLIPL expression, thus inducing TK-10 cell apoptosis.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Proteína Reguladora de Apoptosis Semelhante a CASP8 e FADD/metabolismo
Carcinoma de Células Renais/enzimologia
Carcinoma de Células Renais/patologia
Desoxiadenosinas/farmacologia
MAP Quinase Quinase 7/metabolismo
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Antígenos de Diferenciação/metabolismo
Apoptose/genética
Carcinoma de Células Renais/genética
Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Movimento Celular/genética
Sobrevivência Celular/efeitos dos fármacos
Sobrevivência Celular/genética
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Células HEK293
Seres Humanos
Inflamação/patologia
Proteínas Quinases JNK Ativadas por Mitógeno/metabolismo
Neoplasias Renais/enzimologia
Neoplasias Renais/genética
Neoplasias Renais/patologia
Sistema de Sinalização das MAP Quinases/genética
Masculino
Camundongos Endogâmicos BALB C
Camundongos Nus
NF-kappa B/metabolismo
Óxido Nítrico/metabolismo
Fosforilação/efeitos dos fármacos
Regiões Promotoras Genéticas/genética
Fator de Necrose Tumoral alfa/farmacologia
Regulação para Cima/efeitos dos fármacos
Regulação para Cima/genética
Proteína X Associada a bcl-2/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Differentiation); 0 (CASP8 and FADD-Like Apoptosis Regulating Protein); 0 (Deoxyadenosines); 0 (GADD45B protein, human); 0 (NF-kappa B); 0 (Tumor Necrosis Factor-alpha); 0 (bcl-2-Associated X Protein); 31C4KY9ESH (Nitric Oxide); EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases); EC 2.7.12.2 (MAP Kinase Kinase 7); EC 2.7.12.2 (MAP2K7 protein, human); GZ8VF4M2J8 (cordycepin)
[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:171019
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186489


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[PMID]:28957419
[Au] Autor:Tartour K; Nguyen XN; Appourchaux R; Assil S; Barateau V; Bloyet LM; Burlaud Gaillard J; Confort MP; Escudero-Perez B; Gruffat H; Hong SS; Moroso M; Reynard O; Reynard S; Decembre E; Ftaich N; Rossi A; Wu N; Arnaud F; Baize S; Dreux M; Gerlier D; Paranhos-Baccala G; Volchkov V; Roingeard P; Cimarelli A
[Ad] Endereço:CIRI, Centre International de Recherche en Infectiologie, Lyon, France.
[Ti] Título:Interference with the production of infectious viral particles and bimodal inhibition of replication are broadly conserved antiviral properties of IFITMs.
[So] Source:PLoS Pathog;13(9):e1006610, 2017 Sep.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:IFITMs are broad antiviral factors that block incoming virions in endosomal vesicles, protecting target cells from infection. In the case of HIV-1, we and others reported the existence of an additional antiviral mechanism through which IFITMs lead to the production of virions of reduced infectivity. However, whether this second mechanism of inhibition is unique to HIV or extends to other viruses is currently unknown. To address this question, we have analyzed the susceptibility of a broad spectrum of viruses to the negative imprinting of the virion particles infectivity by IFITMs. The results we have gathered indicate that this second antiviral property of IFITMs extends well beyond HIV and we were able to identify viruses susceptible to the three IFITMs altogether (HIV-1, SIV, MLV, MPMV, VSV, MeV, EBOV, WNV), as well as viruses that displayed a member-specific susceptibility (EBV, DUGV), or were resistant to all IFITMs (HCV, RVFV, MOPV, AAV). The swapping of genetic elements between resistant and susceptible viruses allowed us to point to specificities in the viral mode of assembly, rather than glycoproteins as dominant factors of susceptibility. However, we also show that, contrarily to X4-, R5-tropic HIV-1 envelopes confer resistance against IFITM3, suggesting that viral receptors add an additional layer of complexity in the IFITMs-HIV interplay. Lastly, we show that the overall antiviral effects ascribed to IFITMs during spreading infections, are the result of a bimodal inhibition in which IFITMs act both by protecting target cells from incoming viruses and in driving the production of virions of reduced infectivity. Overall, our study reports for the first time that the negative imprinting of the virion particles infectivity is a conserved antiviral property of IFITMs and establishes IFITMs as a paradigm of restriction factor capable of interfering with two distinct phases of a virus life cycle.
[Mh] Termos MeSH primário: Antígenos de Diferenciação/metabolismo
Vírion
Replicação Viral
[Mh] Termos MeSH secundário: Linhagem Celular
HIV-1/fisiologia
Interações Hospedeiro-Patógeno
Seres Humanos
Internalização do Vírus
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Differentiation)
[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:170929
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006610


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[PMID]:28892747
[Au] Autor:Duan JX; Zhou Y; Zhou AY; Guan XX; Liu T; Yang HH; Xie H; Chen P
[Ad] Endereço:Department of Respiratory Medicine, The Second Xiangya Hospital, Central South University, Changsha 410011, Hunan, China; Research Unit of Respiratory Disease, Central South University, Changsha 410011, Hunan, China; Diagnosis and Treatment Center of Respiratory Disease, Central South University, Ch
[Ti] Título:Calcitonin gene-related peptide exerts anti-inflammatory property through regulating murine macrophages polarization in vitro.
[So] Source:Mol Immunol;91:105-113, 2017 11.
[Is] ISSN:1872-9142
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Acute lung injury (ALI) is a condition resulting from direct or indirect lung injury associated with high mortality and morbidity. The phenotype of macrophages in lung contributes to the pathological progress of ALI. Calcitonin gene-related peptide (CGRP) is one of the most abundant neuropeptides in lung, and attenuates lipopolysaccharide (LPS)-induced ALI in rats. However, the exact effect of CGRP on the activation of macrophages remains unknown. Here we investigate the effect of CGRP on the macrophages activation and inflammation in murine macrophages in vitro. We found that LPS increased the expression of CGRP in a LPS-induced ALI murine model and LPS-stimulated murine macrophages. Although CGRP didn't alter the expression of tumor necrosis factor-α (a marker of pro-inflammatory phenotype of macrophages, M1 macrophages) or Arginase 1 (Arg1, a marker of M2 macrophages) in non-differentiated macrophages, CGRP significantly reduced the NLRP3 and pro-IL-1ß mRNA expression induced by LPS, as well as NLRP3 protein and IL-1ß secretion induced by LPS+ATP in macrophages in vitro. On the other hand, CGRP dramatically enhanced the Arg1 expression and activity induced by IL-4 in the time- and dose-dependent manners. CGRP also promoted the expression of markers of M2 macrophages (IL-10, Fizz1 and Mrc1) induced by IL-4 in murine macrophages. These effects of CGRP were also observed in primary murine peritoneal macrophages. In addition, we found that CGRP regulated macrophages polarization partially through calmodulin, PKC and PKA pathways. Specifically, CGRP could inhibit the degradation of I-κB induced by LPS, and enhance the phosphorylation of STAT6 induced by IL-4 in macrophages. In conclusion, our results indicate that CGRP regulates macrophage polarization and inhibits inflammation in murine macrophages.
[Mh] Termos MeSH primário: Lesão Pulmonar Aguda/imunologia
Peptídeo Relacionado com Gene de Calcitonina/imunologia
Macrófagos/imunologia
[Mh] Termos MeSH secundário: Lesão Pulmonar Aguda/induzido quimicamente
Lesão Pulmonar Aguda/patologia
Animais
Antígenos de Diferenciação/imunologia
Citocinas/imunologia
Modelos Animais de Doenças
Proteínas I-kappa B/imunologia
Lipopolissacarídeos/toxicidade
Macrófagos/patologia
Masculino
Camundongos
Ratos
Fator de Transcrição STAT6/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, Differentiation); 0 (Cytokines); 0 (I-kappa B Proteins); 0 (Lipopolysaccharides); 0 (STAT6 Transcription Factor); 0 (Stat6 protein, mouse); 83652-28-2 (Calcitonin Gene-Related Peptide)
[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:170912
[St] Status:MEDLINE


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[PMID]:28870783
[Au] Autor:Hou W; Yin J; Vogel U; Sun Z; Liang D
[Ad] Endereço:Key Laboratory of Environment and Population Health of Liaoning Education Ministry (Shenyang Medical College), Shenyang 110034, Liaoning Province, People's Republic of China; Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Department of Pathology, Peking
[Ti] Título:19p13.3-GADD45B common variants and 19q13.3-PPP1R13L and 19q13.3-CD3EAP in lung cancer risk among Chinese.
[So] Source:Chem Biol Interact;277:74-78, 2017 Nov 01.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Lung cancer is the most common cause of cancer-related mortality worldwide. The GADD45 gene family plays important roles in a variety of the responses to cell injury including cell cycle checkpoints, apoptosis, DNA repair and anti-tumor immunity. The 19p13.3-GADD45B encoded protein product is involved in apoptosis and inhibiting tumor growth. To evaluate the association of 19p13.3-GADD45B common variants and lung cancer risk, the present study containing 544 Chinese lung cancer cases and 550 cancer-free controls was conducted. Three htSNPs (haplotype-tagging single nucleotide polymorphism) (rs7354, rs14384, and rs3783501) covering 95% of the common haplotype diversity in 19p13.3-GADD45B and interaction of 19p13.3-GADD45B and 19q13.3-PPP1R13L and 19q13.3-CD3EAP variants and smoking-duration were explored. Genotype and allele frequencies and haplotype distributions of the 19p13.3-GADD45B 3 htSNPs were not associated with lung cancer risk after adjustment for smoking status. 19p13.3-GADD45B rs7354 was associated with lung cancer risk among ≤20 (years) smokers [C/A-A/A versus CC, OR (95% CI) = 3.20 (1.11-9.20), P = 0.025] in a dominant model stratified by smoking duration. MDR (multifactor dimensionality reduction) analyses showed that smoking history as main effect and three-way models (smoking duration, 19p13.3-GADD45B rs3783501, 19q13.3-CD3EAP rs967591) (P = 0.001-0.002) indicated statistically significant association with lung cancer risk. The study identified evidence implicating DNA damage response genes on chromosome 19 in etiology of smoke-exposed lung cancer. In conclusion, our findings demonstrate that 19p13.3-GADD45B rs7354 variant and interaction between 19p13.3-GADD45B rs3783501 and 19q13.3-CD3EAP rs967591 may play a role in association with smoke-exposed lung cancer among Chinese. 19p13.3-GADD45B variants should be further evaluated in large prospective studies with molecular pathological annotations of lung cancer.
[Mh] Termos MeSH primário: Antígenos de Diferenciação/genética
Peptídeos e Proteínas de Sinalização Intracelular/genética
Neoplasias Pulmonares/epidemiologia
Neoplasias Pulmonares/genética
Polimorfismo de Nucleotídeo Único
Proteínas Repressoras/genética
Fumar/efeitos adversos
[Mh] Termos MeSH secundário: Adulto
Grupo com Ancestrais do Continente Asiático/genética
Estudos de Casos e Controles
China/epidemiologia
Dano ao DNA
Feminino
Predisposição Genética para Doença
Haplótipos
Seres Humanos
Masculino
Meia-Idade
Estudos Prospectivos
Fatores de Risco
Fumar/epidemiologia
Fumar/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Differentiation); 0 (CD3EAP protein, human); 0 (GADD45B protein, human); 0 (Intracellular Signaling Peptides and Proteins); 0 (PPP1R13L protein, human); 0 (Repressor Proteins)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170906
[St] Status:MEDLINE


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[PMID]:28860190
[Au] Autor:Gamage DG; Leikina E; Quinn ME; Ratinov A; Chernomordik LV; Millay DP
[Ad] Endereço:From the Department of Molecular Cardiovascular Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio 45229 and.
[Ti] Título:Insights into the localization and function of myomaker during myoblast fusion.
[So] Source:J Biol Chem;292(42):17272-17289, 2017 Oct 20.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Multinucleated skeletal muscle fibers form through the fusion of myoblasts during development and regeneration. Previous studies identified myomaker (Tmem8c) as a muscle-specific membrane protein essential for fusion. However, the specific function of myomaker and how its function is regulated are unknown. To explore these questions, we first examined the cellular localization of endogenous myomaker. Two independent antibodies showed that whereas myomaker does localize to the plasma membrane in cultured myoblasts, the protein also resides in the Golgi and post-Golgi vesicles. These results raised questions regarding the precise cellular location of myomaker function and mechanisms that govern myomaker trafficking between these cellular compartments. Using a synchronized fusion assay, we demonstrated that myomaker functions at the plasma membrane to drive fusion. Trafficking of myomaker is regulated by palmitoylation of C-terminal cysteine residues that allows Golgi localization. Moreover, dissection of the C terminus revealed that palmitoylation was not sufficient for complete fusogenic activity suggesting a function for other amino acids within this C-terminal region. Indeed, C-terminal mutagenesis analysis highlighted the importance of a C-terminal leucine for function. These data reveal that myoblast fusion requires myomaker activity at the plasma membrane and is potentially regulated by proper myomaker trafficking.
[Mh] Termos MeSH primário: Antígenos de Diferenciação/metabolismo
Complexo de Golgi/metabolismo
Lipoilação/fisiologia
Fusão de Membrana/fisiologia
Proteínas de Membrana/metabolismo
Proteínas Musculares/metabolismo
Mioblastos Esqueléticos/metabolismo
[Mh] Termos MeSH secundário: Animais
Antígenos de Diferenciação/genética
Linhagem Celular
Complexo de Golgi/genética
Proteínas de Membrana/genética
Camundongos
Proteínas Musculares/genética
Mioblastos Esqueléticos/citologia
Domínios Proteicos
Transporte Proteico/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Differentiation); 0 (Membrane Proteins); 0 (Muscle Proteins); 0 (myomaker protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171028
[Lr] Data última revisão:
171028
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170902
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.811372


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[PMID]:28801234
[Au] Autor:Xu MM; Pu Y; Han D; Shi Y; Cao X; Liang H; Chen X; Li XD; Deng L; Chen ZJ; Weichselbaum RR; Fu YX
[Ad] Endereço:Department of Pathology, University of Texas Southwestern Medical Center, Dallas, TX 75235, USA; Department of Radiation and Cellular Oncology, The Ludwig Center for Metastasis Research, University of Chicago, Chicago, IL 60637, USA.
[Ti] Título:Dendritic Cells but Not Macrophages Sense Tumor Mitochondrial DNA for Cross-priming through Signal Regulatory Protein α Signaling.
[So] Source:Immunity;47(2):363-373.e5, 2017 Aug 15.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Inhibition of cytosolic DNA sensing represents a strategy that tumor cells use for immune evasion, but the underlying mechanisms are unclear. Here we have shown that CD47-signal regulatory protein α (SIRPα) axis dictates the fate of ingested DNA in DCs for immune evasion. Although macrophages were more potent in uptaking tumor DNA, increase of DNA sensing by blocking the interaction of SIRPα with CD47 preferentially occurred in dendritic cells (DCs) but not in macrophages. Mechanistically, CD47 blockade enabled the activation of NADPH oxidase NOX2 in DCs, which in turn inhibited phagosomal acidification and reduced the degradation of tumor mitochondrial DNA (mtDNA) in DCs. mtDNA was recognized by cyclic-GMP-AMP synthase (cGAS) in the DC cytosol, contributing to type I interferon (IFN) production and antitumor adaptive immunity. Thus, our findings have demonstrated how tumor cells inhibit innate sensing in DCs and suggested that the CD47-SIRPα axis is critical for DC-driven antitumor immunity.
[Mh] Termos MeSH primário: Antígenos de Diferenciação/metabolismo
Neoplasias do Colo/imunologia
DNA Mitocondrial/imunologia
Células Dendríticas/imunologia
Proteínas de Membrana/metabolismo
Receptores Imunológicos/metabolismo
[Mh] Termos MeSH secundário: Animais
Anticorpos Bloqueadores/uso terapêutico
Antígeno CD47/imunologia
Antígeno CD47/metabolismo
Células Cultivadas
Neoplasias do Colo/genética
Neoplasias do Colo/terapia
Apresentação Cruzada
Modelos Animais de Doenças
Seres Humanos
Interferon Tipo I/metabolismo
Macrófagos/imunologia
Glicoproteínas de Membrana/metabolismo
Proteínas de Membrana/genética
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
NADPH Oxidase 2
NADPH Oxidases/metabolismo
Nucleotidiltransferases/metabolismo
Transdução de Sinais
Evasão Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Blocking); 0 (Antigens, Differentiation); 0 (CD47 Antigen); 0 (DNA, Mitochondrial); 0 (Interferon Type I); 0 (MPYS protein, mouse); 0 (Membrane Glycoproteins); 0 (Membrane Proteins); 0 (Ptpns1 protein, mouse); 0 (Receptors, Immunologic); 0 (SIRPA protein, human); EC 1.6.3.- (CYBB protein, human); EC 1.6.3.- (NADPH Oxidase 2); EC 1.6.3.- (NADPH Oxidases); EC 2.7.7.- (MB21D1 protein, mouse); EC 2.7.7.- (Nucleotidyltransferases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170813
[St] Status:MEDLINE



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