Base de dados : LILACS
Pesquisa : D12.644.276.200.100 [Categoria DeCS]
Referências encontradas : 3 [refinar]
Mostrando: 1 .. 3   no formato [Detalhado]

página 1 de 1

  1 / 3 LILACS  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Brasil
Texto completo
Id: biblio-837705
Autor: Jia, Peng; Hu, Yu; Li, Gang; Sun, Yuqin; Zhao, Jian; Fu, Jie; Lu, Cuixia; Liu, Bin.
Título: Roles of the ERK1/2 and PI3K/PKB signaling pathways in regulating the expression of extracellular matrix genes in rat pulmonary artery smooth muscle cells
Fonte: Acta cir. bras;32(5):350-358, May 2017. tab, graf.
Idioma: en.
Projeto: Science and Technology Research Foundation of Sichuan Provincial Health Department.
Resumo: Abstract Purpose: To investigate the mechanisms by which PD98059 and LY294002 interfere with the abnormal deposition of extracellular matrix regulated by connective tissue growth factor (CTGF) of rat pulmonary artery smooth muscle cells (PASMCs). Methods: Rat PASMCs were cultured and separated into a control group. Real-time fluorescence quantitative PCR was performed to detect the expression of collagen III and fibronectin mRNA. Immunohistochemistry and western blot analyses were performed to detect the expression of collagen III protein. Results: The expression of collagen III and fibronectin mRNA was greater in PASMCs stimulated with CTGF for 48 h, than in the control group. After 72h of stimulation, the expression of collagen III protein in the PASMCs was greater than in the control. The equivalent gene and protein expression of the CPL group were much more significant. Conclusions: CTGF can stimulate the gene expression of collagen III and fibronectin in PASMCs, which may be one of the factors that promote pulmonary vascular remodeling (PVR) under the conditions of pulmonary arterial hypertension (PAH). PD98059 and LY294002 can inhibit the ERK1/2 and PI3K/PKB signaling pathways, respectively, thus interfering with the biological effects of CTGF. This may be a new way to reduce PAH-PVR.
Descritores: Flavonoides/farmacologia
Cromonas/farmacologia
Fibronectinas/metabolismo
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Colágeno Tipo III/metabolismo
Fator de Crescimento do Tecido Conjuntivo/farmacologia
-Artéria Pulmonar/citologia
Expressão Gênica/efeitos dos fármacos
Células Cultivadas
Regulação da Expressão Gênica
Fibronectinas/genética
Ratos Sprague-Dawley
Fosfatidilinositol 3-Quinases/metabolismo
Modelos Animais
Colágeno Tipo III/genética
Miócitos de Músculo Liso/citologia
Miócitos de Músculo Liso/metabolismo
Proteínas Proto-Oncogênicas c-akt/metabolismo
Fator de Crescimento do Tecido Conjuntivo/metabolismo
Limites: Animais
Masculino
Responsável: BR1.1 - BIREME


  2 / 3 LILACS  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Brasil
Texto completo
Id: lil-576062
Autor: Aguiar, D. P; Coelho-Aguiar, J. M; Abreu, J. G.
Título: CCN2/CTGF silencing blocks cell aggregation in embryonal carcinoma P19 cell
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;44(3):200-205, Mar. 2011. ilus, tab.
Idioma: en.
Resumo: Connective tissue growth factor (CCN2/CTGF) is a matricellular-secreted protein involved in extracellular matrix remodeling. The P19 cell line is an embryonic carcinoma line widely used as a cellular model for differentiation and migration studies. In the present study, we employed an exogenous source of CCN2 and small interference RNA to address the role of CCN2 in the P19 cell aggregation phenomenon. Our data showed that increasing CCN2 protein concentrations from 0.1 to 20 nM decreased the number of cell clusters and dramatically increased cluster size without changing proliferation or cell survival, suggesting that CCN2 induced aggregation. In addition, CCN2 specific silencing inhibited typical P19 cell aggregation, which could be partially rescued by 20 nM CCN2. The present study demonstrates that CCN2 is a key molecule for cell aggregation of embryonic P19 cells.
Descritores: Agregação Celular/efeitos dos fármacos
Proliferação de Células/efeitos dos fármacos
Fator de Crescimento do Tecido Conjuntivo/farmacologia
Células-Tronco de Carcinoma Embrionário/efeitos dos fármacos
-Adesão Celular
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Sobrevivência Celular/fisiologia
Limites: Humanos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


  3 / 3 LILACS  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Brasil
Coletta, Ricardo Della
Texto completo
Id: lil-553905
Autor: Sobral, Lays Martin; Kellermann, Michele Gassen; Graner, Edgard; Martelli-Junior, Hercilio; Coletta, Ricardo Della.
Título: Cyclosporin A-induced gingival overgrowth is not associated with myofibroblast transdifferentiation
Fonte: Braz. oral res;24(2):182-188, Apr.-June 2010. ilus, graf.
Idioma: en.
Resumo: Cyclosporin A (CyA) induces gingival overgrowth via its stimulatory effects on expression of transforming growth factor-beta1 (TGF-â1) and collagen. It is not known whether CyA has a direct effect on gingival fibroblasts or induces its effect indirectly via stimulation of myofibroblast transdifferentiation. The present study was undertaken to examine the in vivo and in vitro effect of CyA on myofibroblast transdifferentiation. Rats were treated for 60 days with a daily subcutaneous injection of CyA, and the gingival overgrowth tissue was analyzed by immunohistochemistry. In vitro, fibroblasts from normal gingiva (NG) were cultured in the presence of different concentrations of CyA, and subjected to semi-quantitative reverse transcriptase-polymerase chain reaction and western blot. Although CyA treatment stimulated TGF-â1 expression by NG fibroblasts, it lacked to induce expression and production of isoform á of smooth muscle actin (á-SMA), the specific myofibroblast marker. The expression levels of connective tissue growth factor (CTGF), which has been considered a key molecule to promote the transdifferentiation of myofibroblasts via TGF-â1 activation, were unaffected by CyA. Our results demonstrate that CyA-induced gingival overgrowth is not associated with activation of myofibroblast transdifferentiation, since CyA is not capable to increase CTGF expression.
Descritores: Transdiferenciação Celular/efeitos dos fármacos
Fator de Crescimento do Tecido Conjuntivo/metabolismo
Ciclosporina/farmacologia
Fibroblastos/efeitos dos fármacos
Crescimento Excessivo da Gengiva/induzido quimicamente
Imunossupressores/farmacologia
-Actinas/metabolismo
Western Blotting
Técnicas de Cultura de Células
Meios de Cultura
Colágeno/metabolismo
Fator de Crescimento do Tecido Conjuntivo/análise
Fibroblastos/citologia
Fibroblastos/metabolismo
Crescimento Excessivo da Gengiva/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Fator de Crescimento Transformador beta1/análise
Fator de Crescimento Transformador beta1/metabolismo
Limites: Adulto
Animais
Humanos
Masculino
Ratos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME



página 1 de 1
   


Refinar a pesquisa
  Base de dados : 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