Base de dados : MEDLINE
Pesquisa : D05.750.078.730 [Categoria DeCS]
Referências encontradas : 15553 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 1556 ir para página                         

  1 / 15553 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29429158
[Au] Autor:Sun M; Liu JG; Weng QY; Yu L; Wang J
[Ad] Endereço:Department of Pathology, Fudan University Shanghai Cancer Center; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China.
[Ti] Título:[Pleomorphic and dedifferentiated leiomyosarcoma: a clinicopathologic analysis].
[So] Source:Zhonghua Bing Li Xue Za Zhi;47(2):87-93, 2018 Feb 08.
[Is] ISSN:0529-5807
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To investigate the clinicopathologic features, differential diagnosis and biological behavior of pleomorphic leiomyosarcoma (PLMS) and dedifferentiated leiomyosarcoma (DLMS). Forty-nine cases were collected from November 2007 to December 2016, including eight that diagnosed at Fudan University Shanghai Cancer Center, and 41 consultation cases. The clinical findings and pathologic features were reviewed. Immunophenotype was obtained in 33 cases and follow-up information was available in 38 cases. There were 22 males and 27 females with ages ranging from 24 to 83 years (mean 52.5 years). Fifteen cases occurred in extremities, 14 in deep body cavity, 11 in the trunk, 4 in the head and neck, 2 in the bladder, and 1 each in the inguinal region, perineum and femoral vein, respectively. Tumor sizes ranged from 3 to 30 cm (mean 9.1 cm). The tumors were composed of at least small foci of typical leiomyosarcoma (LMS) and areas of high-grade pleomorphic/undifferentiated sarcoma. The typical LMS component showed the characteristic morphology of smooth muscle differentiation and was low to intermediate grade in most cases. Pleomorphic areas were mainly composed of atypical spindle and polygonal cells admixed with variable large, bizarre atypical cells and multinuclear giant cells, mostly mimicking undifferentiated pleomorphic sarcoma. The pleomorphic and leiomyosarcomatous areas were usually intermixed, but the demarcation may be distinct or gradual in some cases. The classical LMS component was positive for at least one myogenic marker: α-SMA in 97.0%(32/33), desmin in 72.7%(24/33), H-caldesmon in 90.9% (20/22), MSA in 14/16, and calponin in 15/15 of cases. The pleomorphic sarcoma component was reactive for at least one myogenic marker in 87.9% (29/33) of cases, usually showing focal and less intense immunoreactivity than classical LMS component: α-SMA was positive in 81.8%(27/33), desmin in 48.5%(16/33), H-caldesmon in 72.7% (16/22), MSA in 12/16, and calponin in 11/15 of cases. Based on staining for muscle markers in the pleomorphic component, 29 cases were designated as PLMS, 4 as DLMS. Ki-67 index ranged from 15% to 70% (mean 40%). Follow-up data was available in 38 cases (77.6%), of which 11 patients (28.9%) died of disease, 12 patients were alive with unresectable or recurrent disease, 14 patients were alive with no evidence of disease and another one died of unrelated cause. The median disease-free and overall survival was 6 and 10 months respectively. Twelve patients exhibited local recurrence and 11 developed metastases. The median interval to progression was 8 months. The identification of areas of typical LMS is crucial for accurate diagnosis of PLMS and DLMS. Both PLMS and DLMS show more aggressive behavior and poorer prognosis than ordinary LMS.
[Mh] Termos MeSH primário: Leiomiossarcoma/patologia
Neoplasias Cutâneas/patologia
[Mh] Termos MeSH secundário: Actinas/análise
Adulto
Idoso
Idoso de 80 Anos ou mais
Biomarcadores Tumorais/análise
Proteínas de Ligação ao Cálcio/análise
Proteínas de Ligação a Calmodulina/análise
Diferenciação Celular
China
Desmina/análise
Diagnóstico Diferencial
Extremidades
Feminino
Histiocitoma Fibroso Maligno/química
Histiocitoma Fibroso Maligno/patologia
Seres Humanos
Imuno-Histoquímica
Imunofenotipagem
Leiomiossarcoma/química
Masculino
Proteínas dos Microfilamentos/análise
Meia-Idade
Recidiva Local de Neoplasia
Neoplasias Cutâneas/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ACTA2 protein, human); 0 (Actins); 0 (Biomarkers, Tumor); 0 (Calcium-Binding Proteins); 0 (Calmodulin-Binding Proteins); 0 (Desmin); 0 (Microfilament Proteins); 0 (calponin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180213
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.0529-5807.2018.02.002


  2 / 15553 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27770636
[Au] Autor:Mez J; Chung J; Jun G; Kriegel J; Bourlas AP; Sherva R; Logue MW; Barnes LL; Bennett DA; Buxbaum JD; Byrd GS; Crane PK; Ertekin-Taner N; Evans D; Fallin MD; Foroud T; Goate A; Graff-Radford NR; Hall KS; Kamboh MI; Kukull WA; Larson EB; Manly JJ; Haines JL; Mayeux R; Pericak-Vance MA; Schellenberg GD; Lunetta KL; Farrer LA; Alzheimer's Disease Genetics Consortium
[Ad] Endereço:Department of Neurology, Boston University School of Medicine, Boston, MA, USA; Alzheimer's Disease and CTE Center, Boston University School of Medicine, Boston, MA, USA. Electronic address: jessemez@bu.edu.
[Ti] Título:Two novel loci, COBL and SLC10A2, for Alzheimer's disease in African Americans.
[So] Source:Alzheimers Dement;13(2):119-129, 2017 Feb.
[Is] ISSN:1552-5279
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: African Americans' (AAs) late-onset Alzheimer's disease (LOAD) genetic risk profile is incompletely understood. Including clinical covariates in genetic analyses using informed conditioning might improve study power. METHODS: We conducted a genome-wide association study (GWAS) in AAs employing informed conditioning in 1825 LOAD cases and 3784 cognitively normal controls. We derived a posterior liability conditioned on age, sex, diabetes status, current smoking status, educational attainment, and affection status, with parameters informed by external prevalence information. We assessed association between the posterior liability and a genome-wide set of single-nucleotide polymorphisms (SNPs), controlling for APOE and ABCA7, identified previously in a LOAD GWAS of AAs. RESULTS: Two SNPs at novel loci, rs112404845 (P = 3.8 × 10 ), upstream of COBL, and rs16961023 (P = 4.6 × 10 ), downstream of SLC10A2, obtained genome-wide significant evidence of association with the posterior liability. DISCUSSION: An informed conditioning approach can detect LOAD genetic associations in AAs not identified by traditional GWAS.
[Mh] Termos MeSH primário: Afroamericanos/genética
Doença de Alzheimer/etnologia
Doença de Alzheimer/genética
Loci Gênicos
Proteínas dos Microfilamentos/genética
Transportadores de Ânions Orgânicos Dependentes de Sódio/genética
Polimorfismo de Nucleotídeo Único
Simportadores/genética
[Mh] Termos MeSH secundário: Transportadores de Cassetes de Ligação de ATP/genética
Idoso
Idoso de 80 Anos ou mais
Apolipoproteínas E/genética
Complicações do Diabetes/etnologia
Complicações do Diabetes/genética
Escolaridade
Feminino
Predisposição Genética para Doença
Estudo de Associação Genômica Ampla
Seres Humanos
Masculino
Prevalência
Fumar/etnologia
Fumar/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ABCA7 protein, human); 0 (ATP-Binding Cassette Transporters); 0 (Apolipoproteins E); 0 (Cobl protein, human); 0 (Microfilament Proteins); 0 (Organic Anion Transporters, Sodium-Dependent); 0 (Symporters); 145420-23-1 (sodium-bile acid cotransporter)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161023
[St] Status:MEDLINE


  3 / 15553 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29410425
[Au] Autor:Cervero P; Wiesner C; Bouissou A; Poincloux R; Linder S
[Ad] Endereço:Institut für Medizinische Mikrobiologie, Virologie und Hygiene, Universitätsklinikum Eppendorf, Martinistr. 52, 20246, Hamburg, Germany.
[Ti] Título:Lymphocyte-specific protein 1 regulates mechanosensory oscillation of podosomes and actin isoform-based actomyosin symmetry breaking.
[So] Source:Nat Commun;9(1):515, 2018 02 06.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Subcellular fine-tuning of the actomyosin cytoskeleton is a prerequisite for polarized cell migration. We identify LSP (lymphocyte-specific protein) 1 as a critical regulator of actomyosin contractility in primary macrophages. LSP1 regulates adhesion and migration, including the parameters cell area and speed, and also podosome turnover, oscillation and protrusive force. LSP1 recruits myosin IIA and its regulators, including myosin light chain kinase and calmodulin, and competes with supervillin, a myosin hyperactivator, for myosin regulators, and for actin isoforms, notably ß-actin. Actin isoforms are anisotropically distributed in myosin IIA-expressing macrophages, and contribute to the differential recruitment of LSP1 and supervillin, thus enabling an actomyosin symmetry break, analogous to the situation in cells expressing two myosin II isoforms. Collectively, these results show that the cellular pattern of actin isoforms builds the basis for the differential distribution of two actomyosin machineries with distinct properties, leading to the establishment of discrete zones of actomyosin contractility.
[Mh] Termos MeSH primário: Actinas/metabolismo
Actomiosina/metabolismo
Macrófagos/metabolismo
Mecanotransdução Celular/fisiologia
Proteínas dos Microfilamentos/metabolismo
Podossomos/fisiologia
[Mh] Termos MeSH secundário: Actomiosina/química
Regulação da Expressão Gênica/fisiologia
Seres Humanos
Proteínas de Membrana/genética
Proteínas de Membrana/metabolismo
Proteínas dos Microfilamentos/genética
Miosina não Muscular Tipo IIA/metabolismo
Conformação Proteica
Isoformas de Proteínas
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Actins); 0 (LSP1 protein, human); 0 (Membrane Proteins); 0 (Microfilament Proteins); 0 (Protein Isoforms); 0 (SVIL protein, human); 9013-26-7 (Actomyosin); EC 3.6.1.- (Nonmuscle Myosin Type IIA)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180208
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-018-02904-x


  4 / 15553 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27778404
[Au] Autor:Menzel L; Kleber L; Friedrich C; Hummel R; Dangel L; Winter J; Schmitz K; Tegeder I; Schäfer MK
[Ad] Endereço:Department of Anesthesiology, University Medical Center, Johannes Gutenberg-University, Mainz, Germany.
[Ti] Título:Progranulin protects against exaggerated axonal injury and astrogliosis following traumatic brain injury.
[So] Source:Glia;65(2):278-292, 2017 02.
[Is] ISSN:1098-1136
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In response to traumatic brain injury (TBI) microglia/macrophages and astrocytes release inflammatory mediators with dual effects on secondary brain damage progression. The neurotrophic and anti-inflammatory glycoprotein progranulin (PGRN) attenuates neuronal damage and microglia/macrophage activation in brain injury but mechanisms are still elusive. Here, we studied histopathology, neurology and gene expression of inflammatory markers in PGRN-deficient mice (Grn ) 24 h and 5 days after experimental TBI. Grn mice displayed increased perilesional axonal injury even though the overall brain tissue loss and neurological consequences were similar to wild-type mice. Brain inflammation was elevated in Grn mice as reflected by increased transcription of pro-inflammatory cytokines TNFα, IL-1ß, IL-6, and decreased transcription of the anti-inflammatory cytokine IL-10. However, numbers of Iba1 microglia/macrophages and immigrated CD45 leukocytes were similar at perilesional sites while determination of IgG extravasation suggested stronger impairment of blood brain barrier integrity in Grn compared to wild-type mice. Most strikingly, Grn mice displayed exaggerated astrogliosis 5 days after TBI as demonstrated by anti-GFAP immunohistochemistry and immunoblot. GFAP astrocytes at perilesional sites were immunolabelled for iNOS and TNFα suggesting that pro-inflammatory activation of astrocytes was attenuated by PGRN. Accordingly, recombinant PGRN (rPGRN) attenuated LPS- and cytokine-evoked iNOS and TNFα mRNA expression in cultured astrocytes. Moreover, intracerebroventricular administration of rPGRN immediately before trauma reduced brain damage and neurological deficits, and restored normal levels of cytokine transcription, axonal injury and astrogliosis 5 days after TBI in Grn mice. Our results show that endogenous and recombinant PGRN limit axonal injury and astrogliosis and suggest therapeutic potential of PGRN in TBI. GLIA 2017;65:278-292.
[Mh] Termos MeSH primário: Axônios/patologia
Lesões Encefálicas Traumáticas/complicações
Lesões Encefálicas Traumáticas/patologia
Gliose/etiologia
Gliose/prevenção & controle
Peptídeos e Proteínas de Sinalização Intercelular/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Astrócitos/efeitos dos fármacos
Astrócitos/patologia
Axônios/metabolismo
Barreira Hematoencefálica/patologia
Proteínas de Ligação ao Cálcio/metabolismo
Células Cultivadas
Citocinas/genética
Citocinas/metabolismo
Modelos Animais de Doenças
Expressão Gênica/efeitos dos fármacos
Expressão Gênica/genética
Regulação da Expressão Gênica/efeitos dos fármacos
Regulação da Expressão Gênica/genética
Gliose/patologia
Peptídeos e Proteínas de Sinalização Intercelular/genética
Peptídeos e Proteínas de Sinalização Intercelular/metabolismo
Lipopolissacarídeos/farmacologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Proteínas dos Microfilamentos/metabolismo
Proteínas do Tecido Nervoso/metabolismo
Doenças do Sistema Nervoso/etiologia
Doenças do Sistema Nervoso/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Aif1 protein, mouse); 0 (Calcium-Binding Proteins); 0 (Cytokines); 0 (Grn protein, mouse); 0 (Intercellular Signaling Peptides and Proteins); 0 (Lipopolysaccharides); 0 (Microfilament Proteins); 0 (Nerve Tissue Proteins)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.1002/glia.23091


  5 / 15553 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28742222
[Au] Autor:Lanser AJ; Rezende RM; Rubino S; Lorello PJ; Donnelly DJ; Xu H; Lau LA; Dulla CG; Caldarone BJ; Robson SC; Weiner HL
[Ad] Endereço:Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
[Ti] Título:Disruption of the ATP/adenosine balance in CD39 mice is associated with handling-induced seizures.
[So] Source:Immunology;152(4):589-601, 2017 12.
[Is] ISSN:1365-2567
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Seizures are due to excessive, synchronous neuronal firing in the brain and are characteristic of epilepsy, the fourth most prevalent neurological disease. We report handling-induced and spontaneous seizures in mice deficient for CD39, a cell-surface ATPase highly expressed on microglial cells. CD39 mice with handling-induced seizures had normal input-output curves and paired-pulse ratio measured from hippocampal slices and lacked microgliosis, astrogliosis or overt cell loss in the hippocampus and cortex. As expected, however, the cerebrospinal fluid of CD39 mice contained increased levels of ATP and decreased levels of adenosine. To determine if immune activation was involved in seizure progression, we challenged mice with lipopolysaccharide (LPS) and measured the effect on microglia activation and seizure severity. Systemic LPS challenge resulted in increased cortical staining of Iba1/CD68 and gene array data from purified microglia predicted increased expression of interleukin-8, triggering receptor expressed on myeloid cells 1, p38, pattern recognition receptors, death receptor, nuclear factor-κB , complement, acute phase, and interleukin-6 signalling pathways in CD39 versus CD39 mice. However, LPS treatment did not affect handling-induced seizures. In addition, microglia-specific CD39 deletion in adult mice was not sufficient to cause seizures, suggesting instead that altered expression of CD39 during development or on non-microglial cells such as vascular endothelial cells may promote the seizure phenotype. In summary, we show a correlation between altered extracellular ATP/adenosine ratio and a previously unreported seizure phenotype in CD39 mice. This work provides groundwork for further elucidation of the underlying mechanisms of epilepsy.
[Mh] Termos MeSH primário: Trifosfato de Adenosina/imunologia
Adenosina/imunologia
Apirase/deficiência
Córtex Cerebral/imunologia
Hipocampo/imunologia
Convulsões/imunologia
[Mh] Termos MeSH secundário: Adenosina/genética
Trifosfato de Adenosina/genética
Animais
Antígenos CD/imunologia
Apirase/imunologia
Proteínas de Ligação ao Cálcio/genética
Proteínas de Ligação ao Cálcio/imunologia
Córtex Cerebral/patologia
Hipocampo/patologia
Lipopolissacarídeos/toxicidade
Camundongos
Camundongos Knockout
Proteínas dos Microfilamentos/genética
Proteínas dos Microfilamentos/imunologia
Convulsões/genética
Convulsões/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aif1 protein, mouse); 0 (Antigens, CD); 0 (Calcium-Binding Proteins); 0 (Lipopolysaccharides); 0 (Microfilament Proteins); 8L70Q75FXE (Adenosine Triphosphate); EC 3.6.1.5 (Apyrase); EC 3.6.1.5 (CD39 antigen); K72T3FS567 (Adenosine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE
[do] DOI:10.1111/imm.12798


  6 / 15553 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28457906
[Au] Autor:Üçal M; Haindl MT; Adzemovic MZ; Strasser J; Theisl L; Zeitelhofer M; Kraitsy K; Ropele S; Schäfer U; Fazekas F; Hochmeister S
[Ad] Endereço:Research Unit of Experimental Neurotraumatology, Department of Neurosurgery, Medical University Graz, Auenbruggerplatz 2.2, 8036 Graz, Austria.
[Ti] Título:Widespread cortical demyelination of both hemispheres can be induced by injection of pro-inflammatory cytokines via an implanted catheter in the cortex of MOG-immunized rats.
[So] Source:Exp Neurol;294:32-44, 2017 08.
[Is] ISSN:1090-2430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cortical demyelination is a common finding in patients with chronic multiple sclerosis (MS) and contributes to disease progression and overall disability. The exact pathomechanism that leads to cortical lesions is not clear. Research is limited by the fact that standard animal models of multiple sclerosis do not commonly affect the cortex, or if they do in some variants, the cortical demyelination is rather sparse and already remyelinated within a few days. In an attempt to overcome these limitations we implanted a tissue-compatible catheter into the cortex of Dark Agouti rats. After 14days the rats were immunized with 5µg myelin oligodendrocyte glycoprotein (MOG) in incomplete Freund's Adjuvant, which did not cause any clinical signs but animals developed a stable anti-MOG antibody titer. Then the animals received an injection of proinflammatory cytokines through the catheter. This led to a demyelination of cortical and subcortical areas starting from day 1 in a cone-like pattern spreading from the catheter area towards the subarachnoid space. On day 3 cortical demyelination already expanded to the contralateral hemisphere and reached its peak between days 9-15 after cytokine injection with a widespread demyelination of cortical and subcortical areas of both hemispheres. Clinically the animals showed only discrete signs of fatigue and recovered completely after day 15. Even on day 30 we still were able to detect demyelination in subpial and intracortical areas along with areas of partial and complete remyelination. Loss of cortical myelin was accompanied with marked microglia activation. A second injection of cytokines through the catheter on day 30 led to a second demyelination phase with the same symptoms, but again no detectable motor dysfunction. Suffering of the animals appeared minor compared to standard Experimental Autoimmune Encephalomyelitis and therefore, even long-term observation and repeated demyelination phases seem ethically acceptable.
[Mh] Termos MeSH primário: Córtex Cerebral/patologia
Citocinas/toxicidade
Doenças Desmielinizantes/induzido quimicamente
Doenças Desmielinizantes/patologia
Encefalomielite Autoimune Experimental/patologia
Lateralidade Funcional/fisiologia
[Mh] Termos MeSH secundário: Animais
Proteínas de Ligação ao Cálcio/metabolismo
Caspase 3/metabolismo
Citocinas/metabolismo
Modelos Animais de Doenças
Encefalomielite Autoimune Experimental/induzido quimicamente
Encefalomielite Autoimune Experimental/diagnóstico por imagem
Encefalomielite Autoimune Experimental/imunologia
Fibrina/metabolismo
Adjuvante de Freund/efeitos adversos
Lateralidade Funcional/efeitos dos fármacos
Imunização/efeitos adversos
Lipídeos/efeitos adversos
Masculino
Proteínas dos Microfilamentos/metabolismo
Microscopia Confocal
Atividade Motora
Proteína Proteolipídica de Mielina/metabolismo
Glicoproteína Associada a Mielina/efeitos adversos
Glicoproteína Associada a Mielina/sangue
Proteínas do Tecido Nervoso/metabolismo
Ratos
Estatísticas não Paramétricas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aif1 protein, rat); 0 (Calcium-Binding Proteins); 0 (Cytokines); 0 (Lipids); 0 (Microfilament Proteins); 0 (Myelin Proteolipid Protein); 0 (Myelin-Associated Glycoprotein); 0 (Nerve Tissue Proteins); 0 (incomplete Freund's adjuvant); 9001-31-4 (Fibrin); 9007-81-2 (Freund's Adjuvant); EC 3.4.22.- (Caspase 3)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180218
[Lr] Data última revisão:
180218
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE


  7 / 15553 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29293625
[Au] Autor:Kell MJ; Riccio RE; Baumgartner EA; Compton ZJ; Pecorin PJ; Mitchell TA; Topczewski J; LeClair EE
[Ad] Endereço:Department of Pediatrics, Northwestern University Feinberg School of Medicine / Stanley Manne Children's Research Center, Chicago, Illinois, United States of America.
[Ti] Título:Targeted deletion of the zebrafish actin-bundling protein L-plastin (lcp1).
[So] Source:PLoS One;13(1):e0190353, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Regulation of the cytoskeleton is essential for cell migration in health and disease. Lymphocyte cytosolic protein 1 (lcp1, also called L-plastin) is a hematopoietic-specific actin-bundling protein that is highly conserved in zebrafish, mice and humans. In addition, L-plastin expression is documented as both a genetic marker and a cellular mechanism contributing to the invasiveness of tumors and transformed cell lines. Despite L-plastin's role in both immunity and cancer, in zebrafish there are no direct studies of its function, and no mutant, knockout or reporter lines available. Using CRISPR-Cas9 genome editing, we generated null alleles of zebrafish lcp1 and examined the phenotypes of these fish throughout the life cycle. Our editing strategy used gRNA to target the second exon of lcp1, producing F0 mosaic fish that were outcrossed to wild types to confirm germline transmission. F1 heterozygotes were then sequenced to identify three unique null alleles, here called 'Charlie', 'Foxtrot' and 'Lima'. In silico, each allele truncates the endogenous protein to less than 5% normal size and removes both essential actin-binding domains (ABD1 and ABD2). Although none of the null lines express detectable LCP1 protein, homozygous mutant zebrafish (-/-) can develop and reproduce normally, a finding consistent with that of the L-plastin null mouse (LPL -/-). However, such mice do have a profound immune defect when challenged by lung bacteria. Interestingly, we observed reduced long-term survival of zebrafish lcp1 -/- homozygotes (~30% below the expected numbers) in all three of our knockout lines, with greatest mortality corresponding to the period (4-6 weeks post-fertilization) when the innate immune system is functional, but the adaptive immune system is not yet mature. This suggests that null zebrafish may have reduced capacity to combat opportunistic infections, which are more easily transmissible in the aquatic environment. Overall, our novel mutant lines establish a sound genetic model and an enhanced platform for further studies of L-plastin gene function in hematopoiesis and cancer.
[Mh] Termos MeSH primário: Deleção de Genes
Glicoproteínas de Membrana/genética
Proteínas dos Microfilamentos/genética
Proteínas de Peixe-Zebra/genética
Peixe-Zebra/genética
[Mh] Termos MeSH secundário: Alelos
Sequência de Aminoácidos
Animais
Clonagem Molecular
Repetições Palindrômicas Curtas Agrupadas e Regularmente Espaçadas
Seres Humanos
Camundongos
Homologia de Sequência de Aminoácidos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Membrane Glycoproteins); 0 (Microfilament Proteins); 0 (Zebrafish Proteins); 0 (plastin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180103
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190353


  8 / 15553 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29284006
[Au] Autor:Dai X; Thiagarajan D; Fang J; Shen J; Annam NP; Yang Z; Jiang H; Ju D; Xie Y; Zhang K; Tseng YY; Yang Z; Rishi AK; Li HJ; Yang M; Li L
[Ad] Endereço:Department of Internal Medicine, Wayne State University, Detroit, Michigan, United States of America.
[Ti] Título:SM22α suppresses cytokine-induced inflammation and the transcription of NF-κB inducing kinase (Nik) by modulating SRF transcriptional activity in vascular smooth muscle cells.
[So] Source:PLoS One;12(12):e0190191, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Vascular smooth muscle cell (VSMC) phenotypic modulation is characterized by the downregulation of SMC actin cytoskeleton proteins. Our published study shows that depletion of SM22α (aka SM22, Transgelin, an actin cytoskeleton binding protein) promotes inflammation in SMCs by activating NF-κB signal pathways both in cultured VSMCs and in response to vascular injury. The goal of this study is to investigate the underlying molecular mechanisms whereby SM22 suppresses NF-κB signaling pathways under inflammatory condition. NF-κB inducing kinase (Nik, aka MAP3K14, activated by the LTßR) is a key upstream regulator of NF-κB signal pathways. Here, we show that SM22 overexpression suppresses the expression of NIK and its downstream NF-κB canonical and noncanonical signal pathways in a VSMC line treated with a LTßR agonist. SM22 regulates NIK expression at both transcriptional and the proteasome-mediated post-translational levels in VSMCs depending on the culture condition. By qPCR, chromatin immunoprecipitation and luciferase assays, we found that Nik is a transcription target of serum response factor (SRF). Although SM22 is known to be expressed in the cytoplasm, we found that SM22 is also expressed in the nucleus where SM22 interacts with SRF to inhibit the transcription of Nik and prototypical SRF regulated genes including c-fos and Egr3. Moreover, carotid injury increases NIK expression in Sm22-/- mice, which is partially relieved by adenovirally transduced SM22. These findings reveal for the first time that SM22 is expressed in the nucleus in addition to the cytoplasm of VSMCs to regulate the transcription of Nik and its downstream proinflammatory NF-kB signal pathways as a modulator of SRF during vascular inflammation.
[Mh] Termos MeSH primário: Citocinas/fisiologia
Inflamação/fisiopatologia
Proteínas dos Microfilamentos/fisiologia
Proteínas Musculares/fisiologia
Músculo Liso Vascular/metabolismo
Proteínas Serina-Treonina Quinases/metabolismo
Transcrição Genética
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Camundongos
Proteínas dos Microfilamentos/genética
Proteínas Musculares/genética
Músculo Liso Vascular/citologia
Proteínas Serina-Treonina Quinases/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cytokines); 0 (Microfilament Proteins); 0 (Muscle Proteins); 0 (Tagln protein, mouse); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.25 (NF-kappa B kinase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171229
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190191


  9 / 15553 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29247647
[Au] Autor:Gomez CP; Descoteaux A
[Ad] Endereço:INRS-Institut Armand-Frappier, 531 boul. des Prairies, Laval, QC, H7V 1B7, Canada.
[Ti] Título:Moesin and myosin IIA modulate phagolysosomal biogenesis in macrophages.
[So] Source:Biochem Biophys Res Commun;495(2):1964-1971, 2018 01 08.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Biogenesis of phagolysosomes is central to the elimination of pathogens by macrophages. We previously showed that Src homology region 2 domain-containing phosphatase 1 (SHP-1) participates in the regulation of phagosome maturation. Through proteomics, we identified moesin and the non-muscle myosin-IIA as proteins interacting with SHP-1 during phagocytosis. Silencing of either moesin or myosin IIA with small interfering RNA inhibited phagosomal acidification and recruitment of LAMP-1. Moreover, the intraphagosomal oxidative burst was impaired in the absence of either SHP-1 or myosin IIA but not moesin. Finally, absence of either SHP-1, moesin, or myosin IIA ablated the capacity of macrophages to clear bacterial infection. Collectively, these results implicate both moesin and myosin IIA in the regulation of phagolysosome biogenesis and in host defense against infections.
[Mh] Termos MeSH primário: Escherichia coli/imunologia
Regulação da Expressão Gênica/imunologia
Macrófagos/imunologia
Proteínas dos Microfilamentos/imunologia
Miosina não Muscular Tipo IIA/imunologia
Fagocitose/imunologia
Fagossomos/imunologia
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Feminino
Camundongos
Camundongos Endogâmicos BALB C
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Microfilament Proteins); 144131-77-1 (moesin); EC 3.6.1.- (Nonmuscle Myosin Type IIA)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171217
[St] Status:MEDLINE


  10 / 15553 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29225172
[Au] Autor:Nagahara H; Seno T; Yamamoto A; Obayashi H; Inoue T; Kida T; Nakabayashi A; Kukida Y; Fujioka K; Fujii W; Murakami K; Kohno M; Kawahito Y
[Ad] Endereço:Inflammation and Immunology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
[Ti] Título:Role of allograft inflammatory factor-1 in bleomycin-induced lung fibrosis.
[So] Source:Biochem Biophys Res Commun;495(2):1901-1907, 2018 01 08.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Allograft inflammatory factor-1 (AIF-1) is a protein expressed by macrophages infiltrating the area around the coronary arteries in a rat ectopic cardiac allograft model. We previously reported that AIF-1 is associated with the pathogenesis of rheumatoid arthritis and skin fibrosis in sclerodermatous graft-versus-host disease mice. Here, we used an animal model of bleomycin-induced lung fibrosis to analyze the expression of AIF-1 and examine its function in lung fibrosis. The results showed that AIF-1 was expressed on lung tissues, specifically macrophages, from mice with bleomycin-induced lung fibrosis. Recombinant AIF-1 increased the production of TGF-ß which plays crucial roles in the mechanism of fibrosis by mouse macrophage cell line RAW264.7. Recombinant AIF-1 also increased both the proliferation and migration of lung fibroblasts compared with control group. These results suggest that AIF-1 plays an important role in the mechanism underlying lung fibrosis, and may provide an attractive new therapeutic target.
[Mh] Termos MeSH primário: Bleomicina
Proteínas de Ligação ao Cálcio/imunologia
Fatores Imunológicos/imunologia
Ativação de Macrófagos/imunologia
Macrófagos/imunologia
Proteínas dos Microfilamentos/imunologia
Fibrose Pulmonar/induzido quimicamente
Fibrose Pulmonar/imunologia
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Macrófagos/patologia
Camundongos
Camundongos Endogâmicos C57BL
Fibrose Pulmonar/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Aif1 protein, mouse); 0 (Calcium-Binding Proteins); 0 (Immunologic Factors); 0 (Microfilament Proteins); 11056-06-7 (Bleomycin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE



página 1 de 1556 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

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