Base de dados : MEDLINE
Pesquisa : D09.698.735 [Categoria DeCS]
Referências encontradas : 19515 [refinar]
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[PMID]:27778377
[Au] Autor:Kyyriäinen J; Ekolle Ndode-Ekane X; Pitkänen A
[Ad] Endereço:Department of Neurobiology, A. I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, FI-70211, Finland.
[Ti] Título:Dynamics of PDGFRß expression in different cell types after brain injury.
[So] Source:Glia;65(2):322-341, 2017 02.
[Is] ISSN:1098-1136
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Platelet-derived growth factor receptor ß (PDGFRß) is upregulated after brain injury and its depletion results in the blood-brain barrier (BBB) damage. We investigated the time-window and localization of PDGFRß expression in mice with intrahippocampal kainic acid-induced status epilepticus (SE) and in rats with lateral fluid-percussion-induced traumatic brain injury (TBI). Tissue immunohistochemistry was evaluated at several time-points after SE and TBI. The distribution of PDGFRß was analyzed, and its cell type-specific expression was verified with double/triple-labeling of astrocytes (GFAP), NG2 cells, and endothelial cells (RECA-1). In normal mouse hippocampus, we found evenly distributed PDGFRß+ parenchymal cells. In double-labeling, all NG2+ and 40%-60% GFAP+ cells were PDGFRß+. After SE, PDGFRß+ cells clustered in the ipsilateral hilus (178% of that in controls at fourth day, 225% at seventh day, P < 0.05) and in CA3 (201% at seventh day, P < 0.05), but the total number of PDGFRß+ cells was not altered. As in controls, PDGFRß-immunoreactivity was detected in parenchymal NG2+ and GFAP+ cells. We also observed PDGFRß+ structural pericytes, detached reactive pericytes, and endothelial cells. After TBI, PDGFRß+ cells clustered in the perilesional cortex and thalamus, particularly during the first post-injury week. PDGFRß immunopositivity was observed in NG2+ and GFAP+ cells, structural pericytes, detached reactive pericytes, and endothelial cells. In some animals, PDGFRß vascular staining was observed around the cortical glial scar for up to 3 months. Our data revealed an acute accumulation of PDGFRß+ BBB-related cells in degenerating brain areas, which can be long lasting, suggesting an active role for PDGFRß-signaling in blood vessel and post-injury tissue recovery. GLIA 2017;65:322-341.
[Mh] Termos MeSH primário: Astrócitos/classificação
Astrócitos/metabolismo
Lesões Encefálicas/patologia
Células Endoteliais/metabolismo
Molécula-1 de Adesão Celular Endotelial de Plaquetas/metabolismo
Receptor alfa de Fator de Crescimento Derivado de Plaquetas/metabolismo
[Mh] Termos MeSH secundário: Animais
Antígenos/metabolismo
Modelos Animais de Doenças
Proteína Glial Fibrilar Ácida/metabolismo
Proteínas de Fluorescência Verde/genética
Proteínas de Fluorescência Verde/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Pericitos/metabolismo
Pericitos/patologia
Proteoglicanas/metabolismo
Ratos
Ratos Sprague-Dawley
Receptor alfa de Fator de Crescimento Derivado de Plaquetas/genética
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens); 0 (Glial Fibrillary Acidic Protein); 0 (Platelet Endothelial Cell Adhesion Molecule-1); 0 (Proteoglycans); 0 (chondroitin sulfate proteoglycan 4); 147336-22-9 (Green Fluorescent Proteins); EC 2.7.10.1 (Receptor, Platelet-Derived Growth Factor alpha)
[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.23094


  2 / 19515 MEDLINE  
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[PMID]:28463693
[Au] Autor:Jeon EY; Choi BH; Jung D; Hwang BH; Cha HJ
[Ad] Endereço:Department of Chemical Engineering, Pohang University of Science and Technology, Pohang 790-784, South Korea.
[Ti] Título:Natural healing-inspired collagen-targeting surgical protein glue for accelerated scarless skin regeneration.
[So] Source:Biomaterials;134:154-165, 2017 Jul.
[Is] ISSN:1878-5905
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Skin scarring after deep dermal injuries is a major clinical problem due to the current therapies limited to established scars with poor understanding of healing mechanisms. From investigation of aberrations within the extracellular matrix involved in pathophysiologic scarring, it was revealed that one of the main factors responsible for impaired healing is abnormal collagen reorganization. Here, inspired by the fundamental roles of decorin, a collagen-targeting proteoglycan, in collagen remodeling, we created a scar-preventive collagen-targeting glue consisting of a newly designed collagen-binding mussel adhesive protein and a specific glycosaminoglycan. The collagen-targeting glue specifically bound to type I collagen in a dose-dependent manner and regulated the rate and the degree of fibrillogenesis. In a rat skin excisional model, the collagen-targeting glue successfully accelerated initial wound regeneration as defined by effective reepithelialization, neovascularization, and rapid collagen synthesis. Moreover, the improved dermal collagen architecture was demonstrated by uniform size of collagen fibrils, their regular packing, and a restoration of healthy tissue component. Collectively, our natural healing-inspired collagen-targeting glue may be a promising therapeutic option for improving the healing rate with high-quality and effective scar inhibition.
[Mh] Termos MeSH primário: Colágeno/química
Hidrogel de Polietilenoglicol-Dimetacrilato/química
Adesivos Teciduais/química
Adesivos Teciduais/uso terapêutico
Cicatrização/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Colágeno Tipo I/química
Colágeno Tipo I/uso terapêutico
Decorina/química
Decorina/uso terapêutico
Eletroforese em Gel de Poliacrilamida
Feminino
Glicosaminoglicanos
Seres Humanos
Camundongos
Microscopia Eletrônica de Transmissão
Células NIH 3T3
Proteínas/química
Proteínas/uso terapêutico
Proteoglicanas/química
Proteoglicanas/uso terapêutico
Ratos
Ratos Sprague-Dawley
Pele/efeitos dos fármacos
Pele/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Collagen Type I); 0 (Decorin); 0 (Glycosaminoglycans); 0 (Proteins); 0 (Proteoglycans); 0 (Tissue Adhesives); 0 (adhesive protein, mussel); 25852-47-5 (Hydrogel, Polyethylene Glycol Dimethacrylate); 9007-34-5 (Collagen)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE


  3 / 19515 MEDLINE  
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[PMID]:29395078
[Au] Autor:Han S; Lee JY; Heo EY; Kwon IK; Yune TY; Youn I
[Ad] Endereço:Biomedical Research Institute, Korea Institute of Science and Technology, 5, Hwarang-ro 14-gil, Seongbuk-gu, Seoul, 02791, Republic of Korea.
[Ti] Título:Implantation of a Matrigel-loaded agarose scaffold promotes functional regeneration of axons after spinal cord injury in rat.
[So] Source:Biochem Biophys Res Commun;496(3):785-791, 2018 02 12.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:An agarose scaffold can be useful for supporting and guiding injured axons after spinal cord injury (SCI), but the electrophysiological signal of regenerated axon in scaffolds has not yet been determined. The current study investigated whether a Matrigel-loaded agarose scaffold would enhance the regeneration of axons after SCI. Moreover, the functional connectivity of regenerated axons within the channels of the scaffold was evaluated by directly recording motor evoked potentials. Our data showed that the agarose scaffold containing Matrigel can support and enhance linearly organized axon regeneration after SCI. Additionally, motor evoked potentials were successfully recorded from regenerated axons. These results demonstrate that an agarose scaffold loaded with Matrigel could promote the regeneration of axons and guide the reconnection of functional axons after SCI.
[Mh] Termos MeSH primário: Axônios/patologia
Colágeno/química
Regeneração Tecidual Guiada/instrumentação
Laminina/química
Regeneração Nervosa/fisiologia
Proteoglicanas/química
Traumatismos da Medula Espinal/patologia
Traumatismos da Medula Espinal/terapia
Tecidos Suporte
[Mh] Termos MeSH secundário: Animais
Materiais Biomiméticos/síntese química
Combinação de Medicamentos
Desenho de Equipamento
Análise de Falha de Equipamento
Masculino
Crescimento Neuronal
Próteses e Implantes
Ratos
Ratos Sprague-Dawley
Recuperação de Função Fisiológica
Sefarose/química
Traumatismos da Medula Espinal/fisiopatologia
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Drug Combinations); 0 (Laminin); 0 (Proteoglycans); 119978-18-6 (matrigel); 9007-34-5 (Collagen); 9012-36-6 (Sepharose)
[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:180204
[St] Status:MEDLINE


  4 / 19515 MEDLINE  
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[PMID]:27770219
[Au] Autor:Marshall LE; Koomullil R; Frost AR; Berry JL
[Ad] Endereço:Department of Biomedical Engineering, University of Alabama at Birmingham, Shelby Biomedical Research Bldg. Rm. 802, 1825 University Blvd, Birmingham, AL, 35294, USA.
[Ti] Título:Computational and Experimental Analysis of Fluid Transport Through Three-Dimensional Collagen-Matrigel Hydrogels.
[So] Source:Ann Biomed Eng;45(4):1027-1038, 2017 04.
[Is] ISSN:1573-9686
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A preclinical testing model for cancer therapeutics that replicates in vivo physiology is needed to accurately describe drug delivery and efficacy prior to clinical trials. To develop an in vitro model of breast cancer that mimics in vivo drug/nutrient delivery as well as physiological size and bio-composition, it is essential to describe the mass transport quantitatively. The objective of the present study was to develop in vitro and computational models to measure mass transport from a perfusion system into a 3D extracellular matrix (ECM). A perfusion-flow bioreactor system was used to control and quantify the mass transport of a macromolecule within an ECM hydrogel with embedded through-channels. The material properties, fluid mechanics, and structure of the construct quantified in the in vitro model were input into, and served as validation of, the computational fluid dynamics (CFD) simulation. Results showed that advection and diffusion played a complementary role in mass transport. As the CFD simulation becomes more complex with embedded blood vessels and cancer cells, it will become more recapitulative of in vivo breast cancers. This study is a step toward development of a preclinical testing platform that will be more predictive of patient response to therapeutics than two-dimensional cell culture.
[Mh] Termos MeSH primário: Neoplasias da Mama
Colágeno
Simulação por Computador
Hidrogéis
Laminina
Modelos Biológicos
Neovascularização Patológica
Proteoglicanas
[Mh] Termos MeSH secundário: Transporte Biológico Ativo
Neoplasias da Mama/irrigação sanguínea
Neoplasias da Mama/metabolismo
Neoplasias da Mama/patologia
Combinação de Medicamentos
Feminino
Seres Humanos
Hidrodinâmica
Neovascularização Patológica/metabolismo
Neovascularização Patológica/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Drug Combinations); 0 (Hydrogels); 0 (Laminin); 0 (Proteoglycans); 119978-18-6 (matrigel); 9007-34-5 (Collagen)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161023
[St] Status:MEDLINE
[do] DOI:10.1007/s10439-016-1748-6


  5 / 19515 MEDLINE  
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[PMID]:28464847
[Au] Autor:Rajas O; Quirós LM; Ortega M; Vazquez-Espinosa E; Merayo-Lloves J; Vazquez F; García B
[Ad] Endereço:Pneumology Service, Hospital La Princesa, Institute for Health Research (IP), Hospital Universitario de La Princesa, Madrid, Spain.
[Ti] Título:Glycosaminoglycans are involved in bacterial adherence to lung cells.
[So] Source:BMC Infect Dis;17(1):319, 2017 05 02.
[Is] ISSN:1471-2334
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Lower respiratory infections are among the top ten causes of death worldwide. Since pathogen to cell adhesion is a crucial step in the infection progress, blocking the interaction between eukaryotic receptors and bacterial ligands may enable the pathogenesis process to be stopped. Cell surface glycosaminoglycans (GAGs) are known to be mediators in the adhesion of diverse bacteria to different cell types, making it of interest to examine their involvement in the attachment of various pathogenic bacteria to lung cells, including epithelial cells and fibroblasts. METHODS: The function of cell surface GAGs in bacterial adhesion was studied by reducing their levels through inhibiting their biosynthesis and enzymatic degradation, as well as in binding competition experiments with various species of GAGs. The participation of the different bacterial adhesins in attachment was evaluated through competition with two peptides, both containing consensus heparin binding sequences. Blocking inhibition assays using anti-syndecans and the enzymatic removal of glypicans were conducted to test their involvement in bacterial adhesion. The importance of the fine structure of GAGs in the interaction with pathogens was investigated in competition experiments with specifically desulfated heparins. RESULTS: The binding of all bacteria tested decreased when GAG levels in cell surface of both lung cells were diminished. Competition experiments with different types of GAGs showed that heparan sulfate chains are the main species involved. Blocking or removal of cell surface proteoglycans evidenced that syndecans play a more important role than glypicans. The binding was partially inhibited by peptides including heparin binding sequences. Desulfated heparins also reduced bacterial adhesion to different extents depending on the bacterium and the sulfated residue, especially in fibroblast cells. CONCLUSIONS: Taken together, these data demonstrate that the GAG chains of the cell surface are involved in the adhesion of bacterial adhesins to lung cells. Heparan sulfate seems to be the main species implicated, and binding is dependent on the sulfation pattern of the molecule. These data could facilitate the development of new anti-infective strategies, enabling the development of new procedures for blocking the interaction between pathogens and lung cells more effectively.
[Mh] Termos MeSH primário: Aderência Bacteriana/fisiologia
Glicosaminoglicanos/metabolismo
Bactérias Gram-Positivas/patogenicidade
[Mh] Termos MeSH secundário: Linhagem Celular
Células Epiteliais/microbiologia
Fibroblastos/microbiologia
Heparina/metabolismo
Heparitina Sulfato/metabolismo
Seres Humanos
Pulmão/citologia
Pulmão/microbiologia
Proteoglicanas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Glycosaminoglycans); 0 (Proteoglycans); 9005-49-6 (Heparin); 9050-30-0 (Heparitin Sulfate)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180120
[Lr] Data última revisão:
180120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1186/s12879-017-2418-5


  6 / 19515 MEDLINE  
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[PMID]:27777239
[Au] Autor:Gao X; Lee HY; da Rocha EL; Zhang C; Lu YF; Li D; Feng Y; Ezike J; Elmes RR; Barrasa MI; Cahan P; Li H; Daley GQ; Lodish HF
[Ad] Endereço:Whitehead Institute for Biomedical Research, Cambridge, MA.
[Ti] Título:TGF-ß inhibitors stimulate red blood cell production by enhancing self-renewal of BFU-E erythroid progenitors.
[So] Source:Blood;128(23):2637-2641, 2016 12 08.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Burst-forming unit erythroid progenitors (BFU-Es) are so named based on their ability to generate in methylcellulose culture large colonies of erythroid cells that consist of "bursts" of smaller erythroid colonies derived from the later colony-forming unit erythroid progenitor erythropoietin (Epo)-dependent progenitors. "Early" BFU-E cells forming large BFU-E colonies presumably have higher capacities for self-renewal than do "late" BFU-Es forming small colonies, but the mechanism underlying this heterogeneity remains unknown. We show that the type III transforming growth factor ß (TGF-ß) receptor (TßRIII) is a marker that distinguishes early and late BFU-Es. Transient elevation of TßRIII expression promotes TGF-ß signaling during the early BFU-E to late BFU-E transition. Blocking TGF-ß signaling using a receptor kinase inhibitor increases early BFU-E cell self-renewal and total erythroblast production, suggesting the usefulness of this type of drug in treating Epo-unresponsive anemias.
[Mh] Termos MeSH primário: Antígenos de Diferenciação/metabolismo
Eritrócitos/metabolismo
Células Precursoras Eritroides/metabolismo
Proteoglicanas/metabolismo
Receptores de Fatores de Crescimento Transformadores beta/metabolismo
Transdução de Sinais/fisiologia
Fator de Crescimento Transformador beta/metabolismo
[Mh] Termos MeSH secundário: Anemia/metabolismo
Anemia/terapia
Animais
Eritrócitos/citologia
Células Precursoras Eritroides/citologia
Eritropoetina/metabolismo
Seres Humanos
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, Differentiation); 0 (Proteoglycans); 0 (Receptors, Transforming Growth Factor beta); 0 (Transforming Growth Factor beta); 11096-26-7 (Erythropoietin); 145170-29-2 (betaglycan)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180111
[Lr] Data última revisão:
180111
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE


  7 / 19515 MEDLINE  
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[PMID]:27770373
[Au] Autor:Gómez-Contreras P; Ramiro-Díaz JM; Sierra A; Stipp C; Domann FE; Weigel RJ; Lal G
[Ad] Endereço:Division of Surgical Oncology and Endocrine Surgery, Department of Surgery, University of Iowa, 200 Hawkins Drive, 4641 JCP, Iowa City, IA, 52242, USA.
[Ti] Título:Extracellular matrix 1 (ECM1) regulates the actin cytoskeletal architecture of aggressive breast cancer cells in part via S100A4 and Rho-family GTPases.
[So] Source:Clin Exp Metastasis;34(1):37-49, 2017 01.
[Is] ISSN:1573-7276
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:ECM1 overexpression is an independent predictor of poor prognosis in primary breast carcinomas, however the mechanisms by which ECM1 affects tumor progression have not been completely elucidated. ECM1 was silenced in the triple-negative breast cancer cell lines Hs578T and MDAMB231 using siRNA and the cells were evaluated for changes in morphology, migration, invasion and adhesion. Actin cytoskeleton alterations were evaluated by fluorescent staining and levels of activated Rho GTPases by pull down assays. ECM1 downregulation led to significantly diminished cell migration (p = 0.0005 for Hs578T and p = 0.02 for MDAMB231) and cell adhesion (p < 0.001 for Hs578T and p = 0.01 for MDAMB231). Cell invasion (matrigel) was reduced only in the Hs578T cells (p < 0.01). Silencing decreased the expression of the prometastatic molecules S100A4 and TGFßR2 in both cell lines and CD44 in Hs578T cells. ECM1-silenced cells also exhibited alterations in cell shape and showed bundles of F-actin across the cell (stress fibers) whereas NT-siRNA treated cells showed peripheral membrane ruffling. Downregulation of ECM1 was also associated with an increased F/G actin ratio, when compared to the cells transfected with NT siRNA (p < 0.001 for Hs578T and p < 0.00035 for MDAMB231) and a concomitant decline of activated Rho A in the Hs578T cells. Re-expression of S100A4 in ECM1-silenced cells rescued the phenotype in the Hs578T cells but not the MDAMB231 cells. We conclude that ECM1 is a key player in the metastatic process and regulates the actin cytoskeletal architecture of aggressive breast cancer cells at least in part via alterations in S100A4 and Rho A.
[Mh] Termos MeSH primário: Proteínas da Matriz Extracelular/genética
Proteínas Serina-Treonina Quinases/biossíntese
Receptores de Fatores de Crescimento Transformadores beta/biossíntese
Proteína A4 de Ligação a Cálcio da Família S100/biossíntese
Neoplasias de Mama Triplo Negativas/genética
[Mh] Termos MeSH secundário: Citoesqueleto de Actina/genética
Adesão Celular/genética
Linhagem Celular Tumoral
Movimento Celular/genética
Colágeno
Combinação de Medicamentos
Matriz Extracelular/genética
Proteínas da Matriz Extracelular/biossíntese
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Receptores de Hialuronatos/genética
Laminina
Invasividade Neoplásica/genética
Invasividade Neoplásica/patologia
Proteínas Serina-Treonina Quinases/genética
Proteoglicanas
Receptores de Fatores de Crescimento Transformadores beta/genética
Proteína A4 de Ligação a Cálcio da Família S100/genética
Neoplasias de Mama Triplo Negativas/patologia
Proteínas rho de Ligação ao GTP/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Drug Combinations); 0 (ECM1 protein, human); 0 (Extracellular Matrix Proteins); 0 (Hyaluronan Receptors); 0 (Laminin); 0 (Proteoglycans); 0 (Receptors, Transforming Growth Factor beta); 0 (S100 Calcium-Binding Protein A4); 119978-18-6 (matrigel); 142662-27-9 (S100A4 protein, human); 9007-34-5 (Collagen); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.30 (transforming growth factor-beta type II receptor); EC 3.6.5.2 (rho GTP-Binding Proteins)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:180101
[Lr] Data última revisão:
180101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161023
[St] Status:MEDLINE
[do] DOI:10.1007/s10585-016-9827-5


  8 / 19515 MEDLINE  
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[PMID]:29050936
[Au] Autor:Ortega-Francisco S; de la Fuente-Granada M; Alvarez Salazar EK; Bolaños-Castro LA; Fonseca-Camarillo G; Olguin-Alor R; Alemán-Muench GR; López-Casillas F; Raman C; García-Zepeda EA; Soldevila G
[Ad] Endereço:Departamento de Inmunología, Instituto de Investigaciones Biomédicas, UNAM, Mexico.
[Ti] Título:TßRIII is induced by TCR signaling and downregulated in FoxP3 regulatory T cells.
[So] Source:Biochem Biophys Res Commun;494(1-2):82-87, 2017 Dec 09.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:TGF-ß type III receptor (TßRIII) is a co-receptor for TGFß family members required for high-affinity binding of these ligands to their receptors, potentiating their cellular functions. TGF-ßs, Bone Morphogenetic Proteins (BMP2/4) and Inhibins/Activins regulate different checkpoints during T cell differentiation. We have previously reported that TßRIII modulates T cell development by protecting developing thymocytes from apoptosis, however the role of this co-receptor in peripheral lymphocytes still remains elusive. Here we describe a detailed characterization of TßRIII expression in murine and human lymphocyte subpopulations demonstrating that this co-receptor is significantly expressed in T but not B lymphocytes and among them, preferentially expressed on naïve and central memory T cells. TßRIII was upregulated after TCR stimulation, in parallel to other early activation markers. In contrast, natural and induced Tregs downregulated TßRIII in association with FoxP3 upregulation. Finally, anti-TßRIII blocking experiments demonstrated that TßRIII promotes TGFß-dependent iTreg conversion in vitro, and suggest that this co-receptor may be involved in modulating peripheral T cell tolerance and could be considered as a potential target to boost T cell immune responses.
[Mh] Termos MeSH primário: Proteoglicanas/metabolismo
Receptores de Antígenos de Linfócitos T/metabolismo
Receptores de Fatores de Crescimento Transformadores beta/metabolismo
Linfócitos T Reguladores/imunologia
[Mh] Termos MeSH secundário: Animais
Regulação para Baixo
Fatores de Transcrição Forkhead/metabolismo
Seres Humanos
Memória Imunológica
Técnicas In Vitro
Ativação Linfocitária
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Proteoglicanas/antagonistas & inibidores
Proteoglicanas/genética
Receptores de Fatores de Crescimento Transformadores beta/antagonistas & inibidores
Receptores de Fatores de Crescimento Transformadores beta/genética
Transdução de Sinais
Linfócitos T Reguladores/classificação
Linfócitos T Reguladores/metabolismo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (FOXP3 protein, human); 0 (Forkhead Transcription Factors); 0 (Foxp3 protein, mouse); 0 (Proteoglycans); 0 (Receptors, Antigen, T-Cell); 0 (Receptors, Transforming Growth Factor beta); 145170-29-2 (betaglycan)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171021
[St] Status:MEDLINE


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[PMID]:29019897
[Au] Autor:Lin LY; Yeh YC; Chu CH; Won JGS; Shyr YM; Chao Y; Li CP; Wang SE; Chen MH
[Ad] Endereço:aDivision of Endocrinology and Metabolism, Department of Medicine, Taipei Veterans General Hospital bSchool of Medicine, National Yang-Ming University cDepartment of Pathology and Laboratory Medicine dDivision of Otology, Department of Otorhinolaryngology-Head and Neck Surgery eDivision of General Surgery, Department of Surgery fDepartment of Oncology gDivision of Gastroenterology and Hepatology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan.
[Ti] Título:Endocan expression is correlated with poor progression-free survival in patients with pancreatic neuroendocrine tumors.
[So] Source:Medicine (Baltimore);96(41):e8262, 2017 Oct.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Endocan expression has been reported to be associated with aggressive tumor progression and poor outcomes in various cancers, such as breast cancer, renal cell cancer, lung cancer, gastric cancer, and pituitary adenomas. However, the prognostic significance of endocan in neuroendocrine tumors remains unknown. Thus, the aim of this study was to determine the correlation between endocan expression in pancreatic neuroendocrine tumor (PNET) tissues and progression-free survival. This study included 73 patients with confirmed PNETs who were treated in a single tertiary center in north Taiwan between 1992 and 2015. Immunohistochemical endocan expression and microvessel density (MVD) were examined, and the relationships between these parameters and other clinicopathological characteristics were analyzed. The abovementioned patients were divided into groups according to their endocan expression levels (≥1% or <1%) and median MVDs. Negative endocan expression (P = .002) and a high MVD (P < .001) were significant and favorable prognostic factors for progression-free survival. However, positive endocan expression was significantly associated with a low MVD (P = .037) and tumor mitosis (Ki-67 index) (P = .028). Multivariate Cox regression analysis showed that positive endocan expression (hazard ratio: 4.778, P = .018) and lymph node involvement (hazard ratio: 5.121, P = .005) were independent prognostic factors for tumor recurrence.In conclusion, endocan expression was correlated with poor clinical outcomes in PNETs. Our data indicated that endocan expression may be a reliable marker for predicting tumor recurrence in patients with PNETs.
[Mh] Termos MeSH primário: Proteínas de Neoplasias
Recidiva Local de Neoplasia/patologia
Tumores Neuroendócrinos
Neoplasias Pancreáticas
Proteoglicanas
[Mh] Termos MeSH secundário: Adulto
Idoso
Biomarcadores Tumorais/análise
Biomarcadores Tumorais/genética
Intervalo Livre de Doença
Feminino
Expressão Gênica/genética
Seres Humanos
Masculino
Microvasos/metabolismo
Meia-Idade
Invasividade Neoplásica
Proteínas de Neoplasias/análise
Proteínas de Neoplasias/genética
Recidiva Local de Neoplasia/epidemiologia
Estadiamento de Neoplasias
Neovascularização Patológica/metabolismo
Tumores Neuroendócrinos/diagnóstico
Tumores Neuroendócrinos/genética
Tumores Neuroendócrinos/patologia
Tumores Neuroendócrinos/terapia
Neoplasias Pancreáticas/diagnóstico
Neoplasias Pancreáticas/genética
Neoplasias Pancreáticas/patologia
Neoplasias Pancreáticas/terapia
Prognóstico
Proteoglicanas/análise
Proteoglicanas/genética
Estudos Retrospectivos
Estatística como Assunto
Taiwan/epidemiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (ESM1 protein, human); 0 (Neoplasm Proteins); 0 (Proteoglycans)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171122
[Lr] Data última revisão:
171122
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171012
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000008262


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[PMID]:28973326
[Au] Autor:Zhang Y; Kao WW; Hayashi Y; Zhang L; Call M; Dong F; Yuan Y; Zhang J; Wang YC; Yuka O; Shiraishi A; Liu CY
[Ad] Endereço:School of Optometry, Indiana University, Bloomington, Indiana, United States.
[Ti] Título:Generation and Characterization of a Novel Mouse Line, Keratocan-rtTA (KeraRT), for Corneal Stroma and Tendon Research.
[So] Source:Invest Ophthalmol Vis Sci;58(11):4800-4808, 2017 Sep 01.
[Is] ISSN:1552-5783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose: We created a novel inducible mouse line Keratocan-rtTA (KeraRT) that allows specific genetic modification in corneal keratocytes and tenocytes during development and in adults. Methods: A gene-targeting vector (Kera- IRES2-rtTA3) was constructed and inserted right after the termination codon of the mouse Kera allele via gene targeting techniques. The resulting KeraRT mouse was crossed to tet-O-Hist1H2B-EGFP (TH2B-EGFP) to obtain KeraRT/TH2B-EGFP compound transgenic mice, in which cells expressing Kera are labeled with green fluorescence protein (GFP) by doxycycline (Dox) induction. The expression patterns of GFP and endogenous Kera were examined in KeraRT/TH2B-EGFP. Moreover, KeraRT was bred with tet-O-TGF-α to generate a double transgenic mouse, KeraRT/tet-O-TGF-α, to overexpress TGF-α in corneal keratocytes upon Dox induction. Results: Strong GFP-labeled cells were detected in corneal stroma, limbs, and tail when KeraRT/TH2B-EGFP mice were fed Dox chow. There was no GFP in any single transgenic KeraRT or TH2B-EGFP mouse. Histological analysis showed that GFP in the cornea was limited to stromal keratocytes of KeraRT/TH2B-EGFP, which is consistent with Kera expression. Induction of GFP occurred in 24 hours and reached a plateau by 7 days after Dox induction. GFP could be detected 3-months after induction of KeraRT/TH2B-EGFP. Ectopic expression of TGF-α in corneal keratocytes caused hyperplasia in the corneal epithelium and stroma. Conclusions: The novel Dox inducible KeraRT driver mouse line is a useful genetic tool for gene manipulation and elucidating gene functions in corneal stroma and tendons of limbs and tail during embryonic development, homeostasis and pathogenesis.
[Mh] Termos MeSH primário: Substância Própria/metabolismo
Técnicas de Introdução de Genes
Camundongos Transgênicos/genética
Proteoglicanas/genética
Tendões/metabolismo
[Mh] Termos MeSH secundário: Animais
Ceratócitos da Córnea/metabolismo
Modelos Animais de Doenças
Epitélio Anterior/metabolismo
Técnicas de Inativação de Genes
Vetores Genéticos
Proteínas de Fluorescência Verde/metabolismo
Camundongos
Proteoglicanas/metabolismo
Fator de Crescimento Transformador alfa/genética
Fator de Crescimento Transformador alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Kera protein, mouse); 0 (Proteoglycans); 0 (Transforming Growth Factor alpha); 147336-22-9 (Green Fluorescent Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171004
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.17-22661



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