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[PMID]:29320561
[Au] Autor:Zhao W; Wang X; Sun KH; Zhou L
[Ad] Endereço:Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, New York, United States of America.
[Ti] Título:α-smooth muscle actin is not a marker of fibrogenic cell activity in skeletal muscle fibrosis.
[So] Source:PLoS One;13(1):e0191031, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:α-Smooth muscle actin (α-SMA) is used as a marker for a subset of activated fibrogenic cells, myofibroblasts, which are regarded as important effector cells of tissue fibrogenesis. We address whether α-SMA-expressing myofibroblasts are detectable in fibrotic muscles of mdx5cv mice, a mouse model for Duchenne muscular dystrophy (DMD), and whether the α-SMA expression correlates with the fibrogenic function of intramuscular fibrogenic cells. α-SMA immunostaining signal was not detected in collagen I (GFP)-expressing cells in fibrotic muscles of ColI-GFP/mdx5cv mice, but it was readily detected in smooth muscle cells lining intramuscular blood vessel walls. α-SMA expression was detected by quantitative RT-PCR and Western blot in fibrogenic cells sorted from diaphragm and quadriceps muscles of the ColI-GFP/mdx5cv mice. Consistent with the more severe fibrosis in the ColI-GFP/mdx5cv diaphragm, the fibrogenic cells in the diaphragm exerted a stronger fibrogenic function than the fibrogenic cells in the quadriceps as gauged by their extracellular matrix gene expression. However, both gene and protein expression of α-SMA was lower in the diaphragm fibrogenic cells than in the quadriceps fibrogenic cells in the ColI-GFP/mdx5cv mice. We conclude that myofibroblasts are present in fibrotic skeletal muscles, but their expression of α-SMA is not detectable by immunostaining. The level of α-SMA expression by intramuscular fibrogenic cells does not correlate positively with the level of collagen gene expression or the severity of skeletal muscle fibrosis in the mdx5cv mice. α-SMA is not a functional marker of fibrogenic cells in skeletal muscle fibrosis associated with muscular dystrophy.
[Mh] Termos MeSH primário: Actinas/metabolismo
Biomarcadores/metabolismo
Músculo Esquelético/metabolismo
[Mh] Termos MeSH secundário: Animais
Western Blotting
Fibrose
Camundongos
Camundongos Endogâmicos C57BL
Músculo Esquelético/patologia
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Actins); 0 (Biomarkers); 0 (alpha-smooth muscle actin, mouse)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180111
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191031


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[PMID]:29412224
[Au] Autor:El-Batal AI; Ahmed SF
[Ad] Endereço:National Centre for Radiation Research and Technology - NCRRT, Atomic Energy Authority, Drug Radiation Research Department, Nasr City, Cairo, Egypt.
[Ti] Título:Therapeutic effect of Aloe vera and silver nanoparticles on acid-induced oral ulcer in gamma-irradiated mice.
[So] Source:Braz Oral Res;32:e004, 2018 Feb 05.
[Is] ISSN:1807-3107
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:Radiation combined injury, a life-threatening condition, has higher mortality than simple radiation injury. The aim of the present study was to analyze the efficiency of Aloe vera and silver nanoparticles in improving the healing of ulcerated oral mucosa after irradiation. Thirty male Albino mice were divided into five groups: control, radiation, Aloe vera (AV), silver nanoparticles (NS), and AV+NS. The mice were exposed to whole body 6Gy gamma-radiation. After one hour, 20% acetic acid was injected into the submucosal layer of the lower lip for ulcer induction. The animals received topical treatment with the assigned substances for 5 days. Lip specimens were subjected to hematoxylin and eosin and anti alpha-smooth muscle actin immunohistochemical staining. Results demonstrated occurance of ulcer three days post irradiation in all groups except in the AV+NS group where only epithelial detachment was developed. After seven days, data revealed persistent ulcer in radiation group, and almost normal epithelium in the AV+NS group. A significant reduction of epithelial thickness was detected in all groups at the third day as compared to control. At the seventh day, only the AV+NS group restored the epithelial thickness. Area percent of alpha-smooth muscle actin expression was significantly decreased in radiation group at the third day followed by significant increase at the seventh day. However, all treatment groups showed significant increase in alpha-smooth muscle actin at the third day, which decreased to normal level at the seventh day. Our study demonstrated the efficiency of Aloe vera and silver nanoparticles in enhancing ulcer healing after irradiation.
[Mh] Termos MeSH primário: Aloe/química
Raios gama/efeitos adversos
Nanopartículas Metálicas/uso terapêutico
Úlceras Orais/tratamento farmacológico
Úlceras Orais/etiologia
Lesões Experimentais por Radiação/tratamento farmacológico
Prata/uso terapêutico
[Mh] Termos MeSH secundário: Ácido Acético
Actinas/análise
Administração Tópica
Animais
Células Epiteliais/efeitos dos fármacos
Células Epiteliais/efeitos da radiação
Fibroblastos/efeitos dos fármacos
Imuno-Histoquímica
Masculino
Camundongos
Microscopia Eletrônica de Transmissão
Úlceras Orais/patologia
Lesões Experimentais por Radiação/patologia
Valores de Referência
Reprodutibilidade dos Testes
Fatores de Tempo
Resultado do Tratamento
Cicatrização/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Actins); 0 (alpha-smooth muscle actin, mouse); 3M4G523W1G (Silver); Q40Q9N063P (Acetic Acid)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:180208
[St] Status:MEDLINE


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[PMID]:29188663
[Au] Autor:Lü YH; Ma KJ; Li ZH; Gu J; Bao JY; Yang ZF; Gao J; Zeng Y; Tao L; Chen L
[Ad] Endereço:Shanghai University of Medicine & Health Science, Shanghai 201318, China.
[Ti] Título:[Correlation between RNA Expression Level and Early PMI in Human Brain Tissue].
[So] Source:Fa Yi Xue Za Zhi;32(4):245-249, 2016 Aug.
[Is] ISSN:1004-5619
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:OBJECTIVES: To explore the correlation between the expression levels of several RNA markers in human brain tissue and early postmortem interval (PMI). METHODS: Twelve individuals with known PMI (range from 4.3 to 22.5 h) were selected and total RNA was extracted from brain tissue. Eight commonly used RNA markers were chosen including -actin, GAPDH, RPS29, 18S rRNA, 5S rRNA, U6 snRNA, miRNA-9 and miRNA-125b, and the expression levels were detected in brain tissue by real-time fluorescent quantitative PCR. The internal reference markers with stable expression in early PMI were screened using geNorm software and the relationship between its expression level and some relevant factors such as age, gender and cause of death were analyzed. RNA markers normalized by internal reference were inserted into the mathematic model established by previous research for PMI estimation using R software. Model quality was judged by the error rate calculated with estimated PMI. RESULTS: 5S rRNA, miRNA-9 and miRNA-125b showed quite stable expression and their expression levels had no relation with age, gender and cause of death. The error rate of estimated PMI using -actin was 24.6%, while GAPDH was 41.0%. CONCLUSIONS: 5S rRNA, miRNA-9 and miRNA-125b are suitable as internal reference markers of human brain tissue owing to their stable expression in early PMI. The expression level of -actin correlates well with PMI, which can be used as an additional index for early PMI estimation.
[Mh] Termos MeSH primário: Encéfalo/metabolismo
MicroRNAs/análise
Mudanças Depois da Morte
RNA Nuclear Pequeno/análise
[Mh] Termos MeSH secundário: Actinas/análise
Autopsia
Seres Humanos
Modelos Teóricos
Estabilidade de RNA
RNA Ribossômico 18S/análise
RNA Ribossômico 5S/análise
Reação em Cadeia da Polimerase em Tempo Real
Software
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (MicroRNAs); 0 (RNA, Ribosomal, 18S); 0 (RNA, Ribosomal, 5S); 0 (RNA, Small Nuclear); 0 (U6 small nuclear RNA)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE
[do] DOI:10.3969/j.issn.1004-5619.2016.04.002


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[PMID]:28922779
[Au] Autor:Hanley CJ; Mellone M; Ford K; Thirdborough SM; Mellows T; Frampton SJ; Smith DM; Harden E; Szyndralewiez C; Bullock M; Noble F; Moutasim KA; King EV; Vijayanand P; Mirnezami AH; Underwood TJ; Ottensmeier CH; Thomas GJ
[Ad] Endereço:Cancer Sciences Unit, University of Southampton Faculty of Medicine, Southampton, UK; Genkyotex SA, Plan-les-Ouates, Switzerland; La Jolla Institute for Allergy and Immunology, La Jolla, CA.
[Ti] Título:Targeting the Myofibroblastic Cancer-Associated Fibroblast Phenotype Through Inhibition of NOX4.
[So] Source:J Natl Cancer Inst;110(1), 2018 Jan 01.
[Is] ISSN:1460-2105
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Background: Cancer-associated fibroblasts (CAFs) are tumor-promoting and correlate with poor survival in many cancers, which has led to their emergence as potential therapeutic targets. However, effective methods to manipulate these cells clinically have yet to be developed. Methods: CAF accumulation and prognostic significance in head and neck cancer (oral, n = 260; oropharyngeal, n = 271), and colorectal cancer (n = 56) was analyzed using immunohistochemistry. Mechanisms regulating fibroblast-to-myofibroblast transdifferentiation were investigated in vitro using RNA interference/pharmacological inhibitors followed by polymerase chain reaction (PCR), immunoblotting, immunofluorescence, and functional assays. RNA sequencing/bioinformatics and immunohistochemistry were used to analyze NAD(P)H Oxidase-4 (NOX4) expression in different human tumors. NOX4's role in CAF-mediated tumor progression was assessed in vitro, using CAFs from multiple tissues in Transwell and organotypic culture assays, and in vivo, using xenograft (n = 9-15 per group) and isograft (n = 6 per group) tumor models. All statistical tests were two-sided. Results: Patients with moderate/high levels of myofibroblastic-CAF had a statistically significant decrease in cancer-specific survival rates in each cancer type analyzed (hazard ratios [HRs] = 1.69-7.25, 95% confidence intervals [CIs] = 1.11 to 31.30, log-rank P ≤ .01). Fibroblast-to-myofibroblast transdifferentiation was dependent on a delayed phase of intracellular reactive oxygen species, generated by NOX4, across different anatomical sites and differentiation stimuli. A statistically significant upregulation of NOX4 expression was found in multiple human cancers (P < .001), strongly correlating with myofibroblastic-CAFs (r = 0.65-0.91, adjusted P < .001). Genetic/pharmacological inhibition of NOX4 was found to revert the myofibroblastic-CAF phenotype ex vivo (54.3% decrease in α-smooth muscle actin [α-SMA], 95% CI = 10.6% to 80.9%, P = .009), prevent myofibroblastic-CAF accumulation in vivo (53.2%-79.0% decrease in α-SMA across different models, P ≤ .02) and slow tumor growth (30.6%-64.0% decrease across different models, P ≤ .04). Conclusions: These data suggest that pharmacological inhibition of NOX4 may have broad applicability for stromal targeting across cancer types.
[Mh] Termos MeSH primário: Adenocarcinoma/tratamento farmacológico
Fibroblastos Associados a Câncer/patologia
Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico
Carcinoma de Células Escamosas/tratamento farmacológico
Neoplasias Colorretais/química
Neoplasias Esofágicas/tratamento farmacológico
Neoplasias Pulmonares/tratamento farmacológico
Neoplasias Bucais/química
Miofibroblastos/patologia
NADPH Oxidases/antagonistas & inibidores
Neoplasias Orofaríngeas/química
[Mh] Termos MeSH secundário: Actinas/análise
Adenocarcinoma/química
Adenocarcinoma/genética
Adulto
Idoso
Idoso de 80 Anos ou mais
Animais
Fibroblastos Associados a Câncer/química
Fibroblastos Associados a Câncer/fisiologia
Carcinoma Pulmonar de Células não Pequenas/química
Carcinoma Pulmonar de Células não Pequenas/genética
Carcinoma de Células Escamosas/química
Carcinoma de Células Escamosas/genética
Contagem de Células
Transdiferenciação Celular/efeitos dos fármacos
Transdiferenciação Celular/genética
Neoplasias Colorretais/patologia
Progressão da Doença
Neoplasias Esofágicas/química
Neoplasias Esofágicas/genética
Feminino
Neoplasias de Cabeça e Pescoço/química
Neoplasias de Cabeça e Pescoço/tratamento farmacológico
Neoplasias de Cabeça e Pescoço/genética
Seres Humanos
Neoplasias Pulmonares/química
Neoplasias Pulmonares/genética
Masculino
Camundongos
Meia-Idade
Neoplasias Bucais/patologia
Miofibroblastos/química
NADPH Oxidase 4
NADPH Oxidases/análise
NADPH Oxidases/genética
Transplante de Neoplasias
Neoplasias Orofaríngeas/patologia
Fenótipo
Pirazóis/uso terapêutico
Piridinas/uso terapêutico
Interferência de RNA
Espécies Reativas de Oxigênio/metabolismo
Taxa de Sobrevida
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ACTA2 protein, human); 0 (Actins); 0 (GKT137831); 0 (Pyrazoles); 0 (Pyridines); 0 (Reactive Oxygen Species); EC 1.6.3.- (NADPH Oxidase 4); EC 1.6.3.- (NADPH Oxidases); EC 1.6.3.- (NOX4 protein, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170920
[St] Status:MEDLINE
[do] DOI:10.1093/jnci/djx121


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[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


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[PMID]:28458469
[Au] Autor:Ryu J; Lee JW
[Ad] Endereço:Department of Pharmacy, Research Institute of Pharmaceutical Sciences, Tumor Microenvironment Global Core Research Center, Medicinal Bioconvergence Research Center, College of Pharmacy, Seoul National University, Seoul 08826, Republic of Korea.
[Ti] Título:TM4SF5-Mediated Roles in the Development of Fibrotic Phenotypes.
[So] Source:Mediators Inflamm;2017:5108525, 2017.
[Is] ISSN:1466-1861
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Transmembrane 4 L six family member 5 (TM4SF5) can form tetraspanin-enriched microdomains (TERMs) on the cell's surface. TERMs contain protein-protein complexes comprised of tetraspanins, growth factor receptors, and integrins. These complexes regulate communication between extracellular and intracellular spaces to control diverse cellular functions. TM4SF5 influences the epithelial-mesenchymal transition (EMT), aberrant multilayer cellular growth, drug resistance, enhanced migration and invasion, circulation through the bloodstream, tumor-initiation property, metastasis, and muscle development in zebrafish. Here, current data on TM4SF5's roles in the development of fibrotic phenotypes are reviewed. TM4SF5 is induced by transforming growth factor 1 (TGF 1) signaling via a collaboration with epidermal growth factor receptor (EGFR) activation. TM4SF5, by itself or in concert with other receptors, transduces signals intracellularly. In hepatocytes, TM4SF5 expression regulates cell cycle progression, migration, and expression of extracellular matrix components. In CCl -treated mice, TM4SF5, -smooth muscle actin ( -SMA), and collagen I expression are observed together along the fibrotic septa regions of the liver. These fibrotic phenotypes are diminished by anti-TM4SF5 reagents, such as a specific small compound [TSAHC, 4'-( -toluenesulfonylamido)-4-hydroxychalcone] or a chimeric antibody. This review discusses the antifibrotic strategies that target TM4SF5 and its associated protein networks that regulate the intracellular signaling necessary for fibrotic functions of hepatocytes.
[Mh] Termos MeSH primário: Fibrose/metabolismo
Proteínas de Membrana/metabolismo
[Mh] Termos MeSH secundário: Actinas/metabolismo
Animais
Fibrose/genética
Hepatócitos/metabolismo
Seres Humanos
Proteínas de Membrana/genética
Camundongos
Receptor do Fator de Crescimento Epidérmico/genética
Receptor do Fator de Crescimento Epidérmico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Actins); 0 (Membrane Proteins); 0 (TM4SF5 protein, human); EC 2.7.10.1 (Receptor, Epidermal Growth Factor)
[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:170502
[St] Status:MEDLINE
[do] DOI:10.1155/2017/5108525


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[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


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[PMID]:29388836
[Au] Autor:Kwapiszewska G; Crnkovic S; Stenmark KR
[Ad] Endereço:1 Ludwig Boltzmann Institute for Lung Vascular Research Graz, Austria and.
[Ti] Título:A Twist on Pulmonary Vascular Remodeling: Endothelial to Mesenchymal Transition?
[So] Source:Am J Respir Cell Mol Biol;58(2):140-141, 2018 02.
[Is] ISSN:1535-4989
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Actinas/metabolismo
Endotélio/citologia
Hipertensão Pulmonar/patologia
Proteínas Nucleares/metabolismo
Proteína 1 Relacionada a Twist/metabolismo
Remodelação Vascular/fisiologia
[Mh] Termos MeSH secundário: Transição Epitelial-Mesenquimal/fisiologia
Seres Humanos
[Pt] Tipo de publicação:EDITORIAL
[Nm] Nome de substância:
0 (ACTA2 protein, human); 0 (Actins); 0 (Nuclear Proteins); 0 (TWIST1 protein, human); 0 (Twist-Related Protein 1)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180202
[St] Status:MEDLINE
[do] DOI:10.1165/rcmb.2017-0314ED


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[PMID]:29278699
[Au] Autor:Yamashita A; Kondo K; Kunishima Y; Iseki S; Kondo T; Ota MS
[Ad] Endereço:Laboratory of Anatomy, Physiology and Food Biological Science, Department of Food and Nutrition, Japan Women's University, Bunkyo-ku, Tokyo, Japan.
[Ti] Título:Postnatal development of bitter taste avoidance behavior in mice is associated with ACTIN-dependent localization of bitter taste receptors to the microvilli of taste cells.
[So] Source:Biochem Biophys Res Commun;495(4):2579-2583, 2018 01 22.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bitter taste avoidance behavior (BAB) plays a fundamental role in the avoidance of toxic substances with a bitter taste. However, the molecular basis underlying the development of BAB is unknown. To study critical developmental events by which taste buds turn into functional organs with BAB, we investigated the early phase development of BAB in postnatal mice in response to bitter-tasting compounds, such as quinine and thiamine. Postnatal mice started to exhibit BAB for thiamine and quinine at postnatal day 5 (PD5) and PD7, respectively. Histological analyses of taste buds revealed the formation of microvilli in the taste pores starting at PD5 and the localization of type 2 taste receptor 119 (TAS2R119) at the microvilli at PD6. Treatment of the tongue epithelium with cytochalasin D (CytD), which disturbs ACTIN polymerization in the microvilli, resulted in the loss of TAS2R119 localization at the microvilli and the loss of BAB for quinine and thiamine. The release of ATP from the circumvallate papillae tissue due to taste stimuli was also declined following CytD treatment. These results suggest that the localization of TAS2R119 at the microvilli of taste pores is critical for the initiation of BAB.
[Mh] Termos MeSH primário: Actinas/metabolismo
Aprendizagem da Esquiva/fisiologia
Microvilosidades/metabolismo
Frações Subcelulares/metabolismo
Papilas Gustativas/fisiologia
Paladar/fisiologia
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Feminino
Regulação da Expressão Gênica no Desenvolvimento/fisiologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Distribuição Tecidual
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Actins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171227
[St] Status:MEDLINE


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[PMID]:29254291
[Au] Autor:Omar NN; El-Tawdi AH; Tash RF; Shoukry Y; Mahmoud NA; El Bakly W
[Ad] Endereço:Department of Biochemistry, Faculty of Pharmacy, Modern University for Technology and Information, Cairo, Egypt.
[Ti] Título:Tumor potential in rat wounds after short- and long-term administration of platelet-rich plasma.
[So] Source:J Biol Regul Homeost Agents;31(4):889-899, 2017 Oct-Dec.
[Is] ISSN:0393-974X
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:Platelet-rich plasma (PRP) has been recognized as an effective strategy for tissue regeneration, how-ever, the safety of PRP in wound healing in terms of tumorigenicity has not yet been addressed. Therefore, the aim of this study was to examine the impact of PRP administration on the expression of the inflammatory marker, tenascin-C (TnC) and the myofibroblast markers, α-smooth muscle actin (α-SMA) and vimentin. The immune suppressive response was examined by determining the level of forkhead box protein 3 (Foxp3). PRP was administered for both long-term (two times weekly for four weeks) and short-term (for the fourth week only) post-wounding. Collagen I (col1) and lysyl oxidase (LOX) were used to indicate complete healing, after which any increase in the myofibroblast or in the inflammatory markers would suggest tumor potential. Collagen III (col3), a marker for granulation tissue, was used to remark non-healing. Quantitative real-time reverse transcriptase polymerase chain reaction (QRT-PCR) and Western blot showed that after long-term administration of PRP, the expression of TnC, α-SMA and vimentin was barely detected, while being markedly expressed in the wounded non-treated group and in the short-term administration group. Moreover, the active expression of α-SMA in the two groups was associated positively with the expression of col3 and negatively with the expression of col1. The low expression of Foxp3 after short-term administration relative to the control group indicated active immunity against tumor development. In conclusion, these findings indicate that PRP can be safely used in short- and long-term administration without tumorigenesis concern.
[Mh] Termos MeSH primário: Plasma Rico em Plaquetas/fisiologia
Ferida Cirúrgica/terapia
Cicatrização/fisiologia
[Mh] Termos MeSH secundário: Actinas/genética
Actinas/metabolismo
Animais
Biomarcadores/metabolismo
Carcinogênese
Colágeno Tipo I/genética
Colágeno Tipo I/metabolismo
Colágeno Tipo III/genética
Colágeno Tipo III/metabolismo
Feminino
Fatores de Transcrição Forkhead/genética
Fatores de Transcrição Forkhead/metabolismo
Expressão Gênica
Miofibroblastos/metabolismo
Miofibroblastos/patologia
Ratos
Ratos Sprague-Dawley
Ferida Cirúrgica/genética
Ferida Cirúrgica/metabolismo
Ferida Cirúrgica/patologia
Tenascina/genética
Tenascina/metabolismo
Vimentina/genética
Vimentina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (Biomarkers); 0 (Collagen Type I); 0 (Collagen Type III); 0 (Forkhead Transcription Factors); 0 (Foxp3 protein, rat); 0 (Tenascin); 0 (Vimentin); 0 (smooth muscle actin, rat)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171220
[St] Status:MEDLINE



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