Base de dados : MEDLINE
Pesquisa : D12.644.276.374.687 [Categoria DeCS]
Referências encontradas : 40573 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 4058 ir para página                         

  1 / 40573 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28467316
[Au] Autor:Chen R; Cai X; Ma K; Zhou Y; Wang Y; Jiang T
[Ad] Endereço:The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) and Key Laboratory of Oral Biomedicine Ministry of Education, School and Hospital of Stomatology, Wuhan University, Wuhan, People's Republic of China.
[Ti] Título:The fabrication of double-layered chitosan/gelatin/genipin nanosphere coating for sequential and controlled release of therapeutic proteins.
[So] Source:Biofabrication;9(2):025028, 2017 Jun 01.
[Is] ISSN:1758-5090
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Bone regeneration is a complicated process and includes a number of distinct and sequential stages of coordinated cellular actions under the regulation of multiple growth factors. Therefore, bone grafting materials in which growth factors can be incorporated and released in a programmed order in line with the bone tissue healing process may lead to desirable clinical outcomes. In the present study, a double-layered chitosan/gelatin/genipin (d-CSG/G) nanosphere coating is developed by using layer-by-layer electrophoretic deposition and genipin crosslinking. The surface morphology, physicochemical and mechanical properties of the coatings are explored. Cytochrome C is used as a therapeutic model protein and is successfully loaded on the inner and outer layers of the coating. The protein release can be controlled by the loading position, genipin concentration and thickness of the outer layer. Furthermore, the cell response to the coatings was evaluated. Real-time polymerase chain reactions, immunofluorescence staining and extracellular matrix mineralization assay confirmed that the functions of the loaded growth factor are fully preserved after fabrication. Overall, the d-CSG/G nanosphere coating could be a promising growth factor delivery system to promote bone tissue regeneration.
[Mh] Termos MeSH primário: Biomimética/métodos
Quitosana/química
Materiais Revestidos Biocompatíveis/química
Citocromos c/uso terapêutico
Gelatina/química
Iridoides/química
Nanosferas/química
[Mh] Termos MeSH secundário: Animais
Proteína Morfogenética Óssea 2/química
Calcificação Fisiológica
Bovinos
Reagentes para Ligações Cruzadas/química
Preparações de Ação Retardada
Matriz Extracelular/metabolismo
Imunofluorescência
Células Mesenquimais Estromais/citologia
Nanosferas/ultraestrutura
Osteocalcina/metabolismo
Ratos
Reação em Cadeia da Polimerase em Tempo Real
Proteínas Recombinantes/química
Soluções
Espectroscopia de Infravermelho com Transformada de Fourier
Propriedades de Superfície
Fator de Crescimento Transformador beta/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bone Morphogenetic Protein 2); 0 (Coated Materials, Biocompatible); 0 (Cross-Linking Reagents); 0 (Delayed-Action Preparations); 0 (Iridoids); 0 (Recombinant Proteins); 0 (Solutions); 0 (Transforming Growth Factor beta); 0 (recombinant human bone morphogenetic protein-2); 104982-03-8 (Osteocalcin); 9000-70-8 (Gelatin); 9007-43-6 (Cytochromes c); 9012-76-4 (Chitosan); A3V2NE52YG (genipin)
[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:170504
[St] Status:MEDLINE
[do] DOI:10.1088/1758-5090/aa70c3


  2 / 40573 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28452702
[Au] Autor:Shin JM; Kang JH; Lee SA; Park IH; Lee HM
[Ad] Endereço:Department of Otorhinolaryngology-Head and Neck Surgery, Seoul, South Korea.
[Ti] Título:Effect of doxycycline on epithelial-mesenchymal transition the p38/Smad pathway in respiratory epithelial cells.
[So] Source:Am J Rhinol Allergy;31(2):71-77, 2017 Mar 01.
[Is] ISSN:1945-8932
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Doxycycline has antibacterial and anti-inflammatory effects, and it also suppresses collagen biosynthesis. This study aimed to confirm the effects and mechanism of doxycycline on transforming growth factor (TGF) beta 1 induced epithelial-mesenchymal transition and cell migration in A549 and primary nasal epithelial cells. METHODS: A 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyl-tetrazolium bromide assay and phalloidin-fluorescein isothiocyanate staining were used to evaluate cytotoxicity and cellular morphologic changes. Western blot and immunofluorescence staining were used to determine the expression levels of E-cadherin, vimentin, alpha-smooth muscle actin, fibronectin, phosphorylated Smad2/3, and mitogen-activated protein kinases. Scratch and transwell migration assays were used to assess cellular migration ability. RESULTS: Doxycycline (0-10 µg/mL) had no significant cytotoxic effects in A549 and primary nasal epithelial cells. Increased expression of mesenchymal markers, including vimentin, alpha-smooth muscle actin, and fibronectin in TGF beta 1 induced A549 cells were downregulated by doxycycline treatment. In contrast, E-cadherin expression was upregulated in TGF beta 1 induced A549 cells. An in vitro cell migration assay showed that doxycycline also inhibited the ability of TGF beta 1 induced migration. Doxycycline treatment suppressed the activation of Smad2/3 and p38, whereas its inhibitory effects were similar to each element-specific inhibitor in A549 and primary nasal epithelial cells. CONCLUSION: Doxycycline inhibited TGF beta 1 induced epithelial-to-mesenchymal transition and migration by targeting Smad2/3 and p38 signal pathways in respiratory epithelial cells.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Doxiciclina/farmacologia
Transição Epitelial-Mesenquimal/efeitos dos fármacos
Mucosa Respiratória/efeitos dos fármacos
[Mh] Termos MeSH secundário: Células A549
Caderinas/metabolismo
Movimento Celular/efeitos dos fármacos
Regulação da Expressão Gênica
Seres Humanos
Sistema de Sinalização das MAP Quinases
Cultura Primária de Células
Mucosa Respiratória/patologia
Proteína Smad2/metabolismo
Proteína Smad3/metabolismo
Fator de Crescimento Transformador beta/metabolismo
Vimentina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Cadherins); 0 (Smad2 Protein); 0 (Smad3 Protein); 0 (Transforming Growth Factor beta); 0 (Vimentin); N12000U13O (Doxycycline)
[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:170429
[St] Status:MEDLINE
[do] DOI:10.2500/ajra.2017.31.4410


  3 / 40573 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27773809
[Au] Autor:Jung B; Staudacher JJ; Beauchamp D
[Ad] Endereço:University of Illinois at Chicago, Chicago, Illinois. Electronic address: bjung@uic.edu.
[Ti] Título:Transforming Growth Factor ß Superfamily Signaling in Development of Colorectal Cancer.
[So] Source:Gastroenterology;152(1):36-52, 2017 Jan.
[Is] ISSN:1528-0012
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Transforming growth factor (TGF)-ß cytokines signal via a complex network of pathways to regulate proliferation, differentiation, adhesion, migration, and other functions in many cell types. A high percentage of colorectal tumors contain mutations that disrupt TGF-ß family member signaling. We review how TGF-ß family member signaling is altered during development of colorectal cancer, models of study, interaction of pathways, and potential therapeutic strategies.
[Mh] Termos MeSH primário: Neoplasias Colorretais/genética
Neoplasias Colorretais/metabolismo
Receptores de Fatores de Crescimento Transformadores beta/genética
Transdução de Sinais
Proteínas Smad/genética
Fator de Crescimento Transformador beta/genética
Fator de Crescimento Transformador beta/metabolismo
[Mh] Termos MeSH secundário: Ativinas/metabolismo
Animais
Proteínas Morfogenéticas Ósseas/metabolismo
Neoplasias Colorretais/imunologia
Mutação em Linhagem Germinativa
Homeostase
Seres Humanos
Camundongos
Camundongos Knockout
Receptores de Fatores de Crescimento Transformadores beta/imunologia
Proteínas Smad/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Bone Morphogenetic Proteins); 0 (Receptors, Transforming Growth Factor beta); 0 (Smad Proteins); 0 (Transforming Growth Factor beta); 104625-48-1 (Activins)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


  4 / 40573 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29339718
[Au] Autor:Parfejevs V; Debbache J; Shakhova O; Schaefer SM; Glausch M; Wegner M; Suter U; Riekstina U; Werner S; Sommer L
[Ad] Endereço:Institute of Anatomy, University of Zürich, 8057, Zürich, Switzerland.
[Ti] Título:Injury-activated glial cells promote wound healing of the adult skin in mice.
[So] Source:Nat Commun;9(1):236, 2018 01 16.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cutaneous wound healing is a complex process that aims to re-establish the original structure of the skin and its functions. Among other disorders, peripheral neuropathies are known to severely impair wound healing capabilities of the skin, revealing the importance of skin innervation for proper repair. Here, we report that peripheral glia are crucially involved in this process. Using a mouse model of wound healing, combined with in vivo fate mapping, we show that injury activates peripheral glia by promoting de-differentiation, cell-cycle re-entry and dissemination of the cells into the wound bed. Moreover, injury-activated glia upregulate the expression of many secreted factors previously associated with wound healing and promote myofibroblast differentiation by paracrine modulation of TGF-ß signalling. Accordingly, depletion of these cells impairs epithelial proliferation and wound closure through contraction, while their expansion promotes myofibroblast formation. Thus, injury-activated glia and/or their secretome might have therapeutic potential in human wound healing disorders.
[Mh] Termos MeSH primário: Diferenciação Celular/fisiologia
Neuroglia/fisiologia
Pele/fisiopatologia
Cicatrização/fisiologia
[Mh] Termos MeSH secundário: Animais
Ciclo Celular/genética
Ciclo Celular/fisiologia
Diferenciação Celular/genética
Células Cultivadas
Perfilação da Expressão Gênica
Seres Humanos
Camundongos da Linhagem 129
Camundongos Endogâmicos C57BL
Camundongos Endogâmicos DBA
Camundongos Knockout
Camundongos Transgênicos
Miofibroblastos/metabolismo
Miofibroblastos/fisiologia
Neuroglia/citologia
Neuroglia/metabolismo
Fatores de Transcrição SOXE/genética
Fatores de Transcrição SOXE/metabolismo
Transdução de Sinais/genética
Pele/lesões
Pele/inervação
Fator de Crescimento Transformador beta/genética
Fator de Crescimento Transformador beta/metabolismo
Cicatrização/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (SOXE Transcription Factors); 0 (Sox10 protein, mouse); 0 (Transforming Growth Factor beta)
[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:180118
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-01488-2


  5 / 40573 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29406047
[Au] Autor:Mehta KJ; Coombes JD; Briones-Orta M; Manka PP; Williams R; Patel VB; Syn WK
[Ad] Endereço:Regeneration and Repair Group, The Institute of Hepatology, Foundation for Liver Research, London, UK; Faculty of Life Sciences & Medicine, King's College London, London, UK; Department of Biomedical Sciences, University of Westminster, London, UK.
[Ti] Título:Iron Enhances Hepatic Fibrogenesis and Activates Transforming Growth Factor-ß Signaling in Murine Hepatic Stellate Cells.
[So] Source:Am J Med Sci;355(2):183-190, 2018 02.
[Is] ISSN:1538-2990
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Although excess iron induces oxidative stress in the liver, it is unclear whether it directly activates the hepatic stellate cells (HSC). MATERIALS AND METHODS: We evaluated the effects of excess iron on fibrogenesis and transforming growth factor beta (TGF-ß) signaling in murine HSC. Cells were treated with holotransferrin (0.005-5g/L) for 24 hours, with or without the iron chelator deferoxamine (10µM). Gene expressions (α-SMA, Col1-α1, Serpine-1, TGF-ß, Hif1-α, Tfrc and Slc40a1) were analyzed by quantitative real time-polymerase chain reaction, whereas TfR1, ferroportin, ferritin, vimentin, collagen, TGF-ß RII and phospho-Smad2 proteins were evaluated by immunofluorescence, Western blot and enzyme-linked immunosorbent assay. RESULTS: HSC expressed the iron-uptake protein transferrin receptor 1 (TfR1) and the iron-export protein ferroportin. Holotransferrin upregulated TfR1 expression by 1.8-fold (P < 0.03) and ferritin accumulation (iron storage) by 2-fold (P < 0.01), and activated HSC with 2-fold elevations (P < 0.03) in α-SMA messenger RNA and collagen secretion, and a 1.6-fold increase (P < 0.01) in vimentin protein. Moreover, holotransferrin activated the TGF-ß pathway with TGF-ß messenger RNA elevated 1.6-fold (P = 0.05), and protein levels of TGF-ß RII and phospho-Smad2 increased by 1.8-fold (P < 0.01) and 1.6-fold (P < 0.01), respectively. In contrast, iron chelation decreased ferritin levels by 30% (P < 0.03), inhibited collagen secretion by 60% (P < 0.01), repressed fibrogenic genes α-SMA (0.2-fold; P < 0.05) and TGF-ß (0.4-fold; P < 0.01) and reduced levels of TGF-ß RII and phospho-Smad2 proteins. CONCLUSIONS: HSC express iron-transport proteins. Holotransferrin (iron) activates HSC fibrogenesis and the TGF-ß pathway, whereas iron depletion by chelation reverses this, suggesting that this could be a useful adjunct therapy for patients with fibrosis. Further studies in primary human HSC and animal models are necessary to confirm this.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica
Células Estreladas do Fígado/metabolismo
Ferro/metabolismo
Cirrose Hepática/metabolismo
Transdução de Sinais
Fator de Crescimento Transformador beta/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Ferritinas/biossíntese
Células Estreladas do Fígado/patologia
Cirrose Hepática/patologia
Camundongos
Proteínas Serina-Treonina Quinases/biossíntese
RNA Mensageiro/biossíntese
Receptores da Transferrina/biossíntese
Receptores de Fatores de Crescimento Transformadores beta/biossíntese
Proteína Smad2/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (RNA, Messenger); 0 (Receptors, Transferrin); 0 (Receptors, Transforming Growth Factor beta); 0 (Smad2 Protein); 0 (Smad2 protein, mouse); 0 (Tfrc protein, mouse); 0 (Transforming Growth Factor beta); 9007-73-2 (Ferritins); E1UOL152H7 (Iron); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.30 (transforming growth factor-beta type II receptor)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180207
[St] Status:MEDLINE


  6 / 40573 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29342200
[Au] Autor:Otegbeye F; Ojo E; Moreton S; Mackowski N; Lee DA; de Lima M; Wald DN
[Ad] Endereço:Department of Medicine, Division of Hematology and Oncology, University Hospitals Cleveland Medical Center, Cleveland, Ohio, United States of America.
[Ti] Título:Inhibiting TGF-beta signaling preserves the function of highly activated, in vitro expanded natural killer cells in AML and colon cancer models.
[So] Source:PLoS One;13(1):e0191358, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Natural killer cells harnessed from healthy individuals can be expanded ex vivo using various platforms to produce large doses for adoptive transfer into cancer patients. During such expansion, NK cells are increasingly activated and more efficient at killing cancer cells. Adoptive transfer however introduces these activated cells into a highly immunosuppressive tumor microenvironment mediated in part by excessive transforming growth factor beta (TGF-beta) from both cancer cells and their surrounding stroma. This microenvironment ultimately limits the clinical efficacy of NK cell therapy. In this study, we examined the use of a TGF-beta receptor kinase inhibitor, LY2157299, in preserving the cytotoxic function of ex vivo expanded, highly activated NK cells following sustained exposure to pathologic levels of TGF-beta in vitro and in a liver metastases model of colon cancer. Using myeloid leukemia and colon cancer cell lines, we show that the TGF-beta driven impairment of NK cell cytotoxicity is mitigated by LY2157299. We demonstrate this effect using quantitative cytotoxicity assays as well as by showing a preserved activated phenotype with high NKG2D/CD16 expression and enhanced cytokine production. In a mouse liver metastases model of colon cancer, we observed significantly improved eradication of liver metastases in mice treated with adoptive NK cells combined with LY2157299 compared with mice receiving NK cells or TGF beta inhibition alone. We propose that the therapeutic efficacy of adoptive NK cell therapy clinically will be markedly enhanced by complementary approaches targeting TGF-beta signaling in vivo.
[Mh] Termos MeSH primário: Células Matadoras Naturais/metabolismo
Células Matadoras Naturais/fisiologia
Fator de Crescimento Transformador beta/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Neoplasias do Colo/metabolismo
Citotoxicidade Imunológica/fisiologia
Seres Humanos
Imunoterapia Adotiva/métodos
Neoplasias Hepáticas/patologia
Camundongos
Modelos Biológicos
Proteínas Serina-Treonina Quinases/metabolismo
Receptores de Fatores de Crescimento Transformadores beta/metabolismo
Transdução de Sinais
Fator de Crescimento Transformador beta/metabolismo
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Receptors, Transforming Growth Factor beta); 0 (Transforming Growth Factor beta); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.30 (transforming growth factor-beta type II receptor)
[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:180118
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191358


  7 / 40573 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:29284776
[Au] Autor:Matveeva A; Kovalevska L; Kholodnyuk I; Ivanivskaya T; Kashuba E
[Ad] Endereço:R.E. Kavetsky Institute of Experimental Pathology, Oncology and Radiobiology, NAS of Ukraine, Kyiv 03022, Ukraine.
[Ti] Título:The TGF-beta - SMAD pathway is inactivated in cronic lymphocytic leukemia cells.
[So] Source:Exp Oncol;39(4):286-290, 2017 Dec.
[Is] ISSN:1812-9269
[Cp] País de publicação:Ukraine
[La] Idioma:eng
[Ab] Resumo:AIM: To study the status of the tumor growth factor beta (TGFB) pathway in chronic lymphocytic leukemia (CLL) cells and to uncover molecular details underlying CLL cell genesis. OBJECTS AND METHODS: The study was conducted on peripheral blood samples of patients with CLL using the following methods: RNA isolation, analysis of expression of transcription factors using RT2 profiler assay, bioinformatics analysis of publicly available data bases on expression. RESULTS: We have shown that the TGFB - SMAD canonical pathway is not active in CLL cells. SMAD-responsive genes, such as BCL2L1 (BCL-XL), CCND2 (Cyclin D2), and MYC, are down-regulated in CLL cells compared with peripheral blood B cells of healthy donors. CONCLUSIONS: The TGFB-mediated signaling is not active in CLL cells due to low (or absent) expression of SMAD1, -4, -5, -9, and ATF-3. Expression and phosphorylation status of SMAD2 and -3 should be further elucidated in the future studies.
[Mh] Termos MeSH primário: Leucemia Linfocítica Crônica de Células B/metabolismo
Proteínas Smad/metabolismo
Fator de Crescimento Transformador beta/metabolismo
[Mh] Termos MeSH secundário: Seres Humanos
Transdução de Sinais/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Smad Proteins); 0 (Transforming Growth Factor beta)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171230
[St] Status:MEDLINE


  8 / 40573 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29327472
[Au] Autor:He Y; Xu LL; Feng FE; Wang QM; Zhu XL; Wang CC; Zhang JM; Fu HX; Xu LP; Liu KY; Huang XJ; Zhang XH
[Ad] Endereço:Peking University People's Hospital, Peking University Institute of Haematology, Beijing, China.
[Ti] Título:Mesenchymal stem cell deficiency influences megakaryocytopoiesis through the TNFAIP3/NF-κB/SMAD pathway in patients with immune thrombocytopenia.
[So] Source:Br J Haematol;180(3):395-411, 2018 02.
[Is] ISSN:1365-2141
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Immune thrombocytopenia (ITP) is an autoimmune disease. Mesenchymal stem cells (MSCs) play important roles in the physiology and homeostasis of the haematopoietic system, including supporting megakaryocytic differentiation from CD34 haematopoietic progenitor cells. Tumour necrosis factor alpha-induced protein 3 (TNFAIP3, also termed A20) plays a key role in terminating NF-κB signalling. Human genetic studies showed that the polymorphisms of the TNFAIP3 gene may contribute to ITP susceptibility. In this study, we showed a significant decrease in TNFAIP3 and increase in NF-κB/SMAD7 in ITP-MSCs. In co-cultures with CD34 cells, NF-κB was overexpressed in MSCs from healthy controls (HC-MSCs) after transfection with NFKBIA (IκB)-specific short hairpin (sh)RNAs, resulting in MSC deficiency and a reduction in megakaryocytic differentiation and thrombopoiesis. Knockdown of TNFAIP3 expression using TNFAIP3-specific shRNAs in HC-MSCs affected megakaryocytopoiesis. However, IKBKB knockdown corrected megakaryocytopoiesis inhibition in the ITP-MSCs by decreasing NF-κB expression. Amplified TNFAIP3 expression in ITP-MSCs by TNFAIP3 cDNA can facilitate megakaryocyte differentiation. shRNA-mediated knockdown of SMAD7 expression rescued the impaired MSC function in ITP patients. Therefore, we demonstrate that a pathological reduction in TNFAIP3 levels induced NF-κB/SMAD7 pathway activation, causing a deficiency in MSCs in ITP patients. The ability of ITP-MSCs to support megakaryocytic differentiation and thrombopoiesis of CD34 cells was impaired.
[Mh] Termos MeSH primário: Células Mesenquimais Estromais/metabolismo
NF-kappa B/metabolismo
Púrpura Trombocitopênica Idiopática/etiologia
Púrpura Trombocitopênica Idiopática/metabolismo
Transdução de Sinais
Proteínas Smad/metabolismo
Trombopoese
Proteína 3 Induzida por Fator de Necrose Tumoral alfa/metabolismo
[Mh] Termos MeSH secundário: Biomarcadores
Medula Óssea/patologia
Estudos de Casos e Controles
Diferenciação Celular
Ensaio de Unidades Formadoras de Colônias
Citocinas/biossíntese
Expressão Gênica
Seres Humanos
Imunofenotipagem
Células Mesenquimais Estromais/efeitos dos fármacos
Células Mesenquimais Estromais/patologia
Modelos Biológicos
NF-kappa B/genética
Púrpura Trombocitopênica Idiopática/diagnóstico
Púrpura Trombocitopênica Idiopática/tratamento farmacológico
Transdução de Sinais/efeitos dos fármacos
Proteínas Smad/genética
Trombopoese/efeitos dos fármacos
Trombopoese/genética
Fator de Crescimento Transformador beta/metabolismo
Tretinoína/farmacologia
Proteína 3 Induzida por Fator de Necrose Tumoral alfa/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers); 0 (Cytokines); 0 (NF-kappa B); 0 (Smad Proteins); 0 (Transforming Growth Factor beta); 5688UTC01R (Tretinoin); EC 3.4.19.12 (TNFAIP3 protein, human); EC 3.4.19.12 (Tumor Necrosis Factor alpha-Induced Protein 3)
[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:180113
[St] Status:MEDLINE
[do] DOI:10.1111/bjh.15034


  9 / 40573 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:29254293
[Au] Autor:Di Spigna G; Iannone M; Ladogana P; Salzano S; Ventre M; Covelli B; De Marinis E; Postiglione L
[Ad] Endereço:Department of Translational Medical Sciences, University of Naples “Federico II”, Naples, Italy.
[Ti] Título:Human cardiac multipotent adult stem cells in 3D matrix: new approach of tissue engineering in cardiac regeneration post-infarction.
[So] Source:J Biol Regul Homeost Agents;31(4):911-921, 2017 Oct-Dec.
[Is] ISSN:0393-974X
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:Myocardial infarction is the leading cause of morbidity and mortality in developed countries. It causes a left ventricular dysfunction, mainly due to the loss of functional tissue, resulting in heart failure. New therapies are being developed, using a tissue engineering approach, with the ultimate goal of restoring cardiac function by regenerating and repairing the damaged myocardium. In the present study we investigated the behaviour of a specific population of c-kit positive human cardiac stem cells, called Multipotent Adult Stem Cells (MASCs), grown within three-dimensional collagen scaffolds (3D), to establish whether they could be used in post-infarction cardiac regeneration. We also evaluated the expression levels of the Granulocyte Macrophage-Colony Stimulating Factor Receptor (GM-CSFR) and endoglin, a component of the Transforming Growth Factor beta (TGF-ß) receptor complex. Finally, we also evaluated the expression of the α2ß1integrin. MASCs cultured within 3D collagen matrices are able to proliferate and migrate even in the absence of chemotactic agents and express high levels of factors involved in cell proliferation and migration, such as GM-CSFRα chain and integrins. They therefore represent a promising approach to tissue engineering aimed to restore cardiac function. Our results also suggest a role of GM-CSF in cell proliferation, while TGF-ß does not seem to be relevant.
[Mh] Termos MeSH primário: Células-Tronco Adultas/citologia
Células-Tronco Multipotentes/citologia
Engenharia Tecidual/métodos
Tecidos Suporte
[Mh] Termos MeSH secundário: Células-Tronco Adultas/metabolismo
Técnicas de Cultura de Células
Movimento Celular
Proliferação Celular
Separação Celular
Colágeno/química
Endoglina/genética
Endoglina/metabolismo
Expressão Gênica
Seres Humanos
Integrina alfa2beta1/genética
Integrina alfa2beta1/metabolismo
Células-Tronco Multipotentes/metabolismo
Infarto do Miocárdio
Receptores de Fator Estimulador das Colônias de Granulócitos e Macrófagos/genética
Receptores de Fator Estimulador das Colônias de Granulócitos e Macrófagos/metabolismo
Fator de Crescimento Transformador beta/genética
Fator de Crescimento Transformador beta/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ENG protein, human); 0 (Endoglin); 0 (Integrin alpha2beta1); 0 (Receptors, Granulocyte-Macrophage Colony-Stimulating Factor); 0 (Transforming Growth Factor beta); 9007-34-5 (Collagen)
[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


  10 / 40573 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28468863
[Au] Autor:Liu Z; Sanders AJ; Liang G; Song E; Jiang WG; Gong C
[Ad] Endereço:Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetic and Gene Regulation, Breast Tumor Center, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
[Ti] Título:Hey Factors at the Crossroad of Tumorigenesis and Clinical Therapeutic Modulation of Hey for Anticancer Treatment.
[So] Source:Mol Cancer Ther;16(5):775-786, 2017 May.
[Is] ISSN:1538-8514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hairy and Enhancer-of-split related with YRPW motif (Hey) transcription factors are important regulators of stem cell embryogenesis. Clinical relevance shows that they are also highly expressed in malignant carcinoma. Recent studies have highlighted functions for the Hey factors in tumor metastasis, the maintenance of cancer cell self-renewal, as well as proliferation and the promotion of tumor angiogenesis. Pathways that regulate gene expression, such as Notch and TGFß signaling, are frequently aberrant in numerous cancers. In addition, Hey factors control downstream targets via recruitment of histone deacetylases (HDAC). Targeting these signaling pathways or HDACs may reverse tumor progression and provide clinical benefit for cancer patients. Thus, some small molecular inhibitors or monoclonal antibodies of each of these signaling pathways have been studied in clinical trials. This review focuses on the involvement of Hey proteins in malignant carcinoma progression and provides valuable therapeutic information for anticancer treatment. .
[Mh] Termos MeSH primário: Fatores de Transcrição Hélice-Alça-Hélice Básicos/genética
Carcinogênese/genética
Carcinoma/genética
Proteínas de Ciclo Celular/genética
[Mh] Termos MeSH secundário: Carcinoma/patologia
Proliferação Celular/genética
Histona Desacetilases/genética
Seres Humanos
Metástase Neoplásica
Receptores Notch/genética
Transdução de Sinais/genética
Fator de Crescimento Transformador beta/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Basic Helix-Loop-Helix Transcription Factors); 0 (Cell Cycle Proteins); 0 (HEY1 protein, human); 0 (Receptors, Notch); 0 (Transforming Growth Factor beta); EC 3.5.1.98 (Histone Deacetylases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1158/1535-7163.MCT-16-0576



página 1 de 4058 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

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