Base de dados : MEDLINE
Pesquisa : G04.161.500 [Categoria DeCS]
Referências encontradas : 1227 [refinar]
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  1 / 1227 MEDLINE  
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[PMID]:29198711
[Au] Autor:Xing X; Li Z; Yu Z; Cheng G; Li D; Li Z
[Ad] Endereço:The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) & Key Laboratory of Oral Biomedicine, Ministry of Education, School & Hospital of Stomatology, Wuhan University, Wuhan, China.
[Ti] Título:Effects of connective tissue growth factor (CTGF/CCN2) on condylar chondrocyte proliferation, migration, maturation, differentiation and signalling pathway.
[So] Source:Biochem Biophys Res Commun;495(1):1447-1453, 2018 01 01.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CCN2, also known as connective tissue growth factor (CTGF), is a 38 kDa cysteine-rich extracellular matrix protein that regulates a sequence of cellular functions and participates in multiple complex biological processes, such as chondrogenesis and osteogenesis. In the present study, we provided the first evidence describing the physiological role of CCN2 in condylar chondrocyte proliferation, migration, maturation and differentiation. CCN2 was widely expressed throughout the whole layers of condylar cartilage and predominantly distributed in the proliferative zone. Recombinant CCN2 promoted the proliferation, migration, proteoglycan synthesis and differentiation capacity of isolated condylar chondrocytes. The stimulatory effect of CCN2 on chondrocyte proliferation was associated with the activation of phosphatidylinositol 3-kinase/Akt signalling pathway. The blocking of this pathway by its inhibitor LY294002 impaired the proliferative effect of CCN2 on chondrocytes. These results suggested a novel physiological role of CCN2 in the development of condylar cartilage.
[Mh] Termos MeSH primário: Condrócitos/citologia
Condrócitos/fisiologia
Condrogênese/fisiologia
Fator de Crescimento do Tecido Conjuntivo/metabolismo
Côndilo Mandibular/citologia
Côndilo Mandibular/metabolismo
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular/fisiologia
Crescimento Celular
Movimento Celular/fisiologia
Proliferação Celular/fisiologia
Células Cultivadas
Proteína Oncogênica v-akt/metabolismo
Fosfatidilinositol 3-Quinases/metabolismo
Ratos
Ratos Sprague-Dawley
Transdução de Sinais/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Ctgf protein, rat); 139568-91-5 (Connective Tissue Growth Factor); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Oncogene Protein v-akt)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180105
[Lr] Data última revisão:
180105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171205
[St] Status:MEDLINE


  2 / 1227 MEDLINE  
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[PMID]:28464210
[Au] Autor:Odeleye AOO; Castillo-Avila S; Boon M; Martin H; Coopman K
[Ad] Endereço:Centre for Biological Engineering, Loughborough University, Loughborough LE11 3TU, United Kingdom.
[Ti] Título:Development of an optical system for the non-invasive tracking of stem cell growth on microcarriers.
[So] Source:Biotechnol Bioeng;114(9):2032-2042, 2017 09.
[Is] ISSN:1097-0290
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The emergence of medicinal indications for stem cell therapies has seen a need to develop the manufacturing capacity for adherent cells such as mesenchymal stem cells (MSCs). One such development is in the use of microcarriers, which facilitate enhanced cell densities for adherent stem cell cultures when compared with 2D culture platforms. Given the variety of stem cell expansion systems commercially available, novel methods of non-invasive and automated monitoring of cell number, confluence, and aggregation, within disparate environments, will become imperative to process control, ensuring reliable and consistent performance. The in situ epi-illumination of mouse embryonic fibroblasts and human mesenchymal stem cells attached to Cytodex 1 and 3 microcarriers was achieved using a bespoke microscope. Robust image processing techniques were developed to provide quantitative measurements of confluence, aggregate recognition, and cell number, without the need for fluorescent labeling or cell detachment. Large datasets of cells counted on individual microcarriers were statistically analyzed and compared with NucleoCounter measurements, with an average difference of less than 7% observed from days 0 to 6 of a 12-day culture noted, prior to the onset of aggregation. The developed image acquisition system and post-processing methodologies were successfully applied to dynamically moving colonized microcarriers. The proposed system offers a novel method of cell identification at the individual level, to consistently and accurately assess viable cell number, confluence, and cell distribution, while also minimizing the variability inherent in the current invasive means by which cells adhered to microcarriers are analyzed. Biotechnol. Bioeng. 2017;114: 2032-2042. © 2017 The Authors. Biotechnology and Bioengineering Published by Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Rastreamento de Células/instrumentação
Aumento da Imagem/instrumentação
Transplante de Células-Tronco Mesenquimais/instrumentação
Células Mesenquimais Estromais/citologia
Células Mesenquimais Estromais/fisiologia
Microscopia/instrumentação
Dispositivos Ópticos
[Mh] Termos MeSH secundário: Crescimento Celular
Células Cultivadas
Seres Humanos
Aumento da Imagem/métodos
Miniaturização
Reconhecimento Automatizado de Padrão/métodos
Reprodutibilidade dos Testes
Sensibilidade e Especificidade
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1002/bit.26328


  3 / 1227 MEDLINE  
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[PMID]:29236696
[Au] Autor:Gurvich Y; Leshkowitz D; Barkai N
[Ad] Endereço:Department of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel.
[Ti] Título:Dual role of starvation signaling in promoting growth and recovery.
[So] Source:PLoS Biol;15(12):e2002039, 2017 Dec.
[Is] ISSN:1545-7885
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Growing cells are subject to cycles of nutrient depletion and repletion. A shortage of nutrients activates a starvation program that promotes growth in limiting conditions. To examine whether nutrient-deprived cells prepare also for their subsequent recovery, we followed the transcription program activated in budding yeast transferred to low-phosphate media and defined its contribution to cell growth during phosphate limitation and upon recovery. An initial transcription wave was induced by moderate phosphate depletion that did not affect cell growth. A second transcription wave followed when phosphate became growth limiting. The starvation program contributed to growth only in the second, growth-limiting phase. Notably, the early response, activated at moderate depletion, promoted recovery from starvation by increasing phosphate influx upon transfer to rich medium. Our results suggest that cells subject to nutrient depletion prepare not only for growth in the limiting conditions but also for their predicted recovery once nutrients are replenished.
[Mh] Termos MeSH primário: Crescimento Celular
Fosfatos/metabolismo
[Mh] Termos MeSH secundário: Meios de Cultura
Proteínas de Ligação a DNA/genética
Proteínas de Ligação a DNA/metabolismo
Regulação Fúngica da Expressão Gênica
Simportadores de Próton-Fosfato/genética
Simportadores de Próton-Fosfato/metabolismo
Proteínas de Saccharomyces cerevisiae/genética
Proteínas de Saccharomyces cerevisiae/metabolismo
Saccharomycetales
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Culture Media); 0 (DNA-Binding Proteins); 0 (PHO4 protein, S cerevisiae); 0 (PHO84 protein, S cerevisiae); 0 (Phosphates); 0 (Proton-Phosphate Symporters); 0 (Saccharomyces cerevisiae Proteins)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171224
[Lr] Data última revisão:
171224
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171214
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pbio.2002039


  4 / 1227 MEDLINE  
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[PMID]:28768836
[Au] Autor:Horiuchi H; Usami A; Shirai R; Harada N; Ikushiro S; Sakaki T; Nakano Y; Inui H; Yamaji R
[Ad] Endereço:Division of Applied Life Sciences, Graduate School of Life and Environmental Sciences.
[Ti] Título:-Equol Activates cAMP Signaling at the Plasma Membrane of INS-1 Pancreatic ß-Cells and Protects against Streptozotocin-Induced Hyperglycemia by Increasing ß-Cell Function in Male Mice.
[So] Source:J Nutr;147(9):1631-1639, 2017 Sep.
[Is] ISSN:1541-6100
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:-equol, which is enantioselectively produced from daidzein by gut microbiota, has been suggested as a chemopreventive agent against type 2 diabetes mellitus (T2DM), but the underlying mechanisms remain unclear. We investigated the effects of -equol on pancreatic ß-cell function. ß-Cell growth and insulin secretion were evaluated with male Institute of Cancer Research mice and isolated pancreatic islets from the mice, respectively. The mechanisms by which -equol stimulated ß-cell response were examined in INS-1 ß-cells. The effect of -equol treatment on ß-cell function was assessed in low-dose streptozotocin-treated mice. -equol was used at 10 µmol/L for in vitro and ex vivo studies and was administered by oral gavage (20 mg/kg, 2 times/d throughout the experimental period) for in vivo studies. -equol administration for 7 d increased Ki67-positive ß-cells by 27% ( < 0.01) in mice. -equol enantioselectively enhanced glucose-stimulated insulin secretion in mouse pancreatic islets by 41% ( < 0.001). In INS-1 cells, -equol exerted stronger effects than daidzein on cell growth, insulin secretion, and cAMP-response element (CRE)-mediated transcription. These -equol effects were diminished by inhibiting protein kinase A. The effective concentration of -equol for stimulating cAMP production at the plasma membrane was lower than that for phosphodiesterase inhibition. -equol-stimulated CRE activation was negatively controlled by the knockdown of G-protein α subunit group S (stimulatory) and positively controlled by that of G-protein-coupled receptor kinase-3 and -6. Compared with vehicle-treated controls, -equol gavage treatment resulted in an increase in ß-cell mass of 104% ( < 0.05), a trend toward high plasma insulin concentrations (by 118%; = 0.06), and resistance to hyperglycemia after streptozotocin treatment (78% of AUC after glucose challenge; < 0.01). -equol administration significantly increased the number of Ki67-positive proliferating ß-cells by 62% ( < 0.01) and decreased that of terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling-positive apoptotic ß-cells by 75% ( < 0.05). Our results show that -equol boosts ß-cell function and prevents hypoglycemia in mice, suggesting its potential for T2DM prevention.
[Mh] Termos MeSH primário: Glicemia/metabolismo
Membrana Celular/efeitos dos fármacos
AMP Cíclico/metabolismo
Diabetes Mellitus Experimental/tratamento farmacológico
Equol/farmacologia
Células Secretoras de Insulina/efeitos dos fármacos
Insulina/secreção
[Mh] Termos MeSH secundário: Animais
Área Sob a Curva
Crescimento Celular/efeitos dos fármacos
Membrana Celular/metabolismo
Diabetes Mellitus Experimental/sangue
Diabetes Mellitus Experimental/patologia
Diabetes Mellitus Tipo 2/sangue
Diabetes Mellitus Tipo 2/prevenção & controle
Hiperglicemia/sangue
Hiperglicemia/induzido quimicamente
Hiperglicemia/etiologia
Hiperglicemia/prevenção & controle
Células Secretoras de Insulina/citologia
Células Secretoras de Insulina/metabolismo
Isoflavonas/metabolismo
Isoflavonas/farmacologia
Masculino
Camundongos Endogâmicos ICR
Ratos
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Insulin); 0 (Isoflavones); 531-95-3 (Equol); 6287WC5J2L (daidzein); E0399OZS9N (Cyclic AMP)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170913
[Lr] Data última revisão:
170913
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170804
[St] Status:MEDLINE
[do] DOI:10.3945/jn.117.250860


  5 / 1227 MEDLINE  
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[PMID]:28700911
[Au] Autor:Rowghanian P; Campàs O
[Ad] Endereço:Department of Mechanical Engineering and California NanoSystems Institute, University of California, Santa Barbara, Santa Barbara, California.
[Ti] Título:Non-equilibrium Membrane Homeostasis in Expanding Cellular Domains.
[So] Source:Biophys J;113(1):132-137, 2017 Jul 11.
[Is] ISSN:1542-0086
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Many cell behaviors involve cell-shape transformations that impose considerable changes in the cell's surface area, requiring a constant adaptation of the cell's plasma membrane area to prevent cell lysis. Here, we theoretically describe the interplay between the plasma membrane dynamics and a physically connected cell cortex or wall, accounting for spatial variations in membrane recycling and tension. In-plane membrane net flows result naturally from these dynamics and, in the presence of an expanding cell cortex or wall, regions of converging or diverging flow patterns emerge. These flow patterns can potentially explain the spatial localization/segregation of membrane proteins in processes such as cell polarization. We also identify the relevant parameters that control membrane homeostasis and derive the range of parameters for which homeostatic states exist.
[Mh] Termos MeSH primário: Crescimento Celular
Membrana Celular/metabolismo
Homeostase/fisiologia
[Mh] Termos MeSH secundário: Animais
Parede Celular/metabolismo
Endocitose/fisiologia
Exocitose/fisiologia
Modelos Biológicos
Tensão Superficial
Leveduras
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170713
[St] Status:MEDLINE


  6 / 1227 MEDLINE  
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[PMID]:28591610
[Au] Autor:Zhao ZL; Liu ZY; Du J; Xu GK; Feng XQ
[Ad] Endereço:AML, Department of Engineering Mechanics, Institute of Biomechanics and Medical Engineering, Tsinghua University, Beijing, China; Center for Nano and Micro Mechanics, Tsinghua University, Beijing, China.
[Ti] Título:A Dynamic Biochemomechanical Model of Geometry-Confined Cell Spreading.
[So] Source:Biophys J;112(11):2377-2386, 2017 Jun 06.
[Is] ISSN:1542-0086
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cell spreading is involved in many physiological and pathological processes. The spreading behavior of a cell significantly depends on its microenvironment, but the biochemomechanical mechanisms of geometry-confined cell spreading remain unclear. A dynamic model is here established to investigate the spreading of cells confined in a finite region with different geometries, e.g., rectangle, ellipse, triangle, and L-shape. This model incorporates both biophysical and biochemical mechanisms, including actin polymerization, integrin-mediated binding, plasma viscoelasticity, and the elasticity of membranes and microtubules. We simulate the dynamic configurational evolution of a cell under different geometric microenvironments, including the angular distribution of microtubule forces and the deformation of the nucleus. The results indicate that the positioning of the cell-division plane is affected by its boundary confinement: a cell divides in a plane perpendicular to its minimal principal axis of inertia of area. In addition, the effects of such physical factors as the adhesive bond density, membrane tension, and microtubule number are examined on the cell spreading dynamics. The theoretical predictions show a good agreement with relevant experimental results. This work sheds light on the geometry-confined spreading dynamics of cells and holds potential applications in regulating cell division and designing cell-based sensors.
[Mh] Termos MeSH primário: Crescimento Celular
Modelos Biológicos
[Mh] Termos MeSH secundário: Actinas/metabolismo
Animais
Divisão Celular/fisiologia
Núcleo Celular/fisiologia
Simulação por Computador
Elasticidade
Integrinas/metabolismo
Microtúbulos/metabolismo
Tensão Superficial
Viscosidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (Integrins)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170814
[Lr] Data última revisão:
170814
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170608
[St] Status:MEDLINE


  7 / 1227 MEDLINE  
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[PMID]:28552527
[Au] Autor:Yao J; Zuo H; Gao J; Wang M; Wang D; Li X
[Ad] Endereço:State Key Laboratory of Agrobiotechnology, College of Biological Sciences, China Agricultural University, Beijing, China.
[Ti] Título:The effects of IGF-1 on mouse spermatogenesis using an organ culture method.
[So] Source:Biochem Biophys Res Commun;491(3):840-847, 2017 Sep 23.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Currently available organ culture methods can induce the differentiation of spermatogonial stem cells (SSCs) to spermatids in vitro, but the percentages of haploid cells and elongated spermatids are extremely low. The goal of this study was to test strategies to increase the differentiation rate of SSCs into elongated spermatids in vitro. RNA-seq was performed from forty round spermatids isolated by laser capture microdissection from cultured mouse testicular fragments (MTFs) or 27 days post-partum testes. Gene Ontology (GO) and KEGG analysis of the transcriptome revealed that many cell cycle and apoptosis-associated genes were among the differently expressed genes. Quantitative real-time PCR confirmed that the expression of Ccnd3 decreased and the expression of Trp53, Casp8 and Cyct increased in round spermatids from cultured MTFs. As insulin-like growth factor (IGF-1) can regulate cell cycle and apoptosis of many kinds of cells, the expression of Igf-1 decreased in cultured MTFs and IGF-1 receptor expressed strongly in germ cells, IGF-1 was added to the basal medium. IGF-1 increased the percentages of round and elongated spermatids by decreasing the apoptosis of germ cells and increasing the density of germ cells in cultured MTFs. These results indicate that IGF-1 plays a critical role in spermatogenesis from SSCs.
[Mh] Termos MeSH primário: Apoptose/fisiologia
Fator de Crescimento Insulin-Like I/metabolismo
Técnicas de Cultura de Órgãos/métodos
Espermátides/fisiologia
Espermatogênese/fisiologia
Testículo/metabolismo
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Crescimento Celular
Células Cultivadas
Feminino
Técnicas In Vitro
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Modelos Animais
Espermátides/citologia
Testículo/citologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
67763-96-6 (Insulin-Like Growth Factor I)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170912
[Lr] Data última revisão:
170912
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170530
[St] Status:MEDLINE


  8 / 1227 MEDLINE  
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[PMID]:28546423
[Au] Autor:Alejandro EU; Bozadjieva N; Blandino-Rosano M; Wasan MA; Elghazi L; Vadrevu S; Satin L; Bernal-Mizrachi E
[Ad] Endereço:Division of Metabolism, Endocrinology & Diabetes, Department of Internal Medicine, University of Michigan, Ann Arbor, MI.
[Ti] Título:Overexpression of Kinase-Dead mTOR Impairs Glucose Homeostasis by Regulating Insulin Secretion and Not ß-Cell Mass.
[So] Source:Diabetes;66(8):2150-2162, 2017 Aug.
[Is] ISSN:1939-327X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Regulation of glucose homeostasis by insulin depends on ß-cell growth and function. Nutrients and growth factor stimuli converge on the conserved protein kinase mechanistic target of rapamycin (mTOR), existing in two complexes, mTORC1 and mTORC2. To understand the functional relevance of mTOR enzymatic activity in ß-cell development and glucose homeostasis, we generated mice overexpressing either one or two copies of a kinase-dead mTOR mutant (KD-mTOR) transgene exclusively in ß-cells. We examined glucose homeostasis and ß-cell function of these mice fed a control chow or high-fat diet. Mice with two copies of the transgene [RIPCre;KD-mTOR (Homozygous)] develop glucose intolerance due to a defect in ß-cell function without alterations in ß-cell mass with control chow. Islets from RIPCre;KD-mTOR (Homozygous) mice showed reduced mTORC1 and mTORC2 signaling along with transcripts and protein levels of Pdx-1. Islets with reduced mTORC2 signaling in their ß-cells (RIPCre;Rictor ) also showed reduced Pdx-1. When challenged with a high-fat diet, mice carrying one copy of KD-mTOR mutant transgene developed glucose intolerance and ß-cell insulin secretion defect but showed no changes in ß-cell mass. These findings suggest that the mTOR-mediated signaling pathway is not essential to ß-cell growth but is involved in regulating ß-cell function in normal and diabetogenic conditions.
[Mh] Termos MeSH primário: Intolerância à Glucose/genética
Glucose/metabolismo
Células Secretoras de Insulina/metabolismo
Complexos Multiproteicos/metabolismo
Serina-Treonina Quinases TOR/metabolismo
[Mh] Termos MeSH secundário: Animais
Crescimento Celular
Dieta Hiperlipídica/efeitos adversos
Expressão Gênica/fisiologia
Homeostase/fisiologia
Insulina/metabolismo
Células Secretoras de Insulina/citologia
Alvo Mecanístico do Complexo 1 de Rapamicina
Alvo Mecanístico do Complexo 2 de Rapamicina
Camundongos
Camundongos Transgênicos
Proteínas Quinases/deficiência
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Insulin); 0 (Multiprotein Complexes); EC 2.7.- (Protein Kinases); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 1); EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 2); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170527
[St] Status:MEDLINE
[do] DOI:10.2337/db16-1349


  9 / 1227 MEDLINE  
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[PMID]:28422872
[Au] Autor:Zhang Y; Wang J; Ji H; Lu H; Lu L; Wang J; Li Y
[Ad] Endereço:Department of General Surgery, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.
[Ti] Título:Effect of HSP27 and Cofilin in the injury of hypoxia/reoxygenation on hepatocyte membrane F-actin microfilaments.
[So] Source:Medicine (Baltimore);96(16):e6658, 2017 Apr.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hypoxia-reoxygenation (H/R) injury hepatocyte models were established to simulate the ischemia/reperfusion injury of transplanted organ. Through the study of the molecular mechanism of H/R on the F-actin damage of the liver cytomembrane, the mechanism of F-actin damage induced by ischemia and reperfusion was studied from the level of cell and molecule.The hypoxic environment of cells in vitro was simulated by chemical hypoxia agent CoCl2. Liver cells were detected by MTT, H/R group was subdivided into 3 subgroups: H/R 2, 4, and 6 h. Changes of cell shape and the growth state, apoptosis, ultrastructural changes, and the changes in F-actin microfilament content were observed. Heat shock protein 27 (HSP27), Cofilin, and F-actin gene and protein levels were determined by real-time polymerase chain reaction and western blot assay, respectively.Cells showed circular adherence growth under normal circumstances, while the spindle cells and shedding cells were significantly increased in H/R groups. Apoptosis cells in H/R group were increased significantly with the extension of hypoxia time. The number of endoplasmic reticulum was decreased significantly in the H/R group, the mitochondrion hydropic was degenerated and the glycogen was disappeared. The F-actin fibers in the H/R group were disordered, the morphology of the fibers was obviously decreased, and the fluorescence staining decreased obviously (P < .05). The transcription and expression levels of HSP27, Cofilin, and F-actin were significantly lower than those in the control group (P < .05).These results demonstrate that H/R can affect the correct assembly of F-actin microfilaments and weakens the normal cycle of F-actin microfilaments through inhibiting the protein expression and gene transcription of HSP27 and Cofilin in hepatocytes, thereby changing the skeleton of F-actin microfilaments.
[Mh] Termos MeSH primário: Fatores de Despolimerização de Actina/biossíntese
Actinas/biossíntese
Proteínas de Choque Térmico HSP27/biossíntese
Hepatócitos/efeitos dos fármacos
Traumatismo por Reperfusão/patologia
[Mh] Termos MeSH secundário: Animais
Apoptose
Crescimento Celular
Forma Celular
Modelos Animais de Doenças
Hepatócitos/metabolismo
Hepatócitos/ultraestrutura
Seres Humanos
RNA Mensageiro
Ratos
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (Actin Depolymerizing Factors); 0 (Actins); 0 (HSP27 Heat-Shock Proteins); 0 (RNA, Messenger)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170509
[Lr] Data última revisão:
170509
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170420
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000006658


  10 / 1227 MEDLINE  
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[PMID]:28408430
[Au] Autor:Carroll B; Dunlop EA
[Ad] Endereço:Institute for Cell and Molecular Biosciences, Newcastle University, Newcastle upon Tyne, U.K.
[Ti] Título:The lysosome: a crucial hub for AMPK and mTORC1 signalling.
[So] Source:Biochem J;474(9):1453-1466, 2017 Apr 13.
[Is] ISSN:1470-8728
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Much attention has recently been focussed on the lysosome as a signalling hub. Following the initial discovery that localisation of the nutrient-sensitive kinase, mammalian target of rapamycin complex 1 (mTORC1), to the lysosome was essential for mTORC1 activation, the field has rapidly expanded to reveal the role of the lysosome as a platform permitting the co-ordination of several homeostatic signalling pathways. Much is now understood about how the lysosome contributes to amino acid sensing by mTORC1, the involvement of the energy-sensing kinase, AMP-activated protein kinase (AMPK), at the lysosome and how both AMPK and mTORC1 signalling pathways feedback to lysosomal biogenesis and regeneration following autophagy. This review will cover the classical role of the lysosome in autophagy, the dynamic signalling interactions which take place on the lysosomal surface and the multiple levels of cross-talk which exist between lysosomes, AMPK and mTORC1.
[Mh] Termos MeSH primário: Proteínas Quinases Ativadas por AMP/metabolismo
Lisossomos/metabolismo
Complexos Multiproteicos/metabolismo
Transdução de Sinais/fisiologia
Serina-Treonina Quinases TOR/metabolismo
[Mh] Termos MeSH secundário: Animais
Autofagia/fisiologia
Crescimento Celular
Homeostase/fisiologia
Seres Humanos
Alvo Mecanístico do Complexo 1 de Rapamicina
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Multiprotein Complexes); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 1); EC 2.7.11.31 (AMP-Activated Protein Kinases)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170415
[St] Status:MEDLINE
[do] DOI:10.1042/BCJ20160780



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