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Pesquisa : D12.644.276.200.100 [Categoria DeCS]
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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 Celular/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: Seres Humanos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


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Coletta, Ricardo Della
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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
Seres Humanos
Masculino
Ratos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME



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