Base de dados : LILACS
Pesquisa : G04.198 [Categoria DeCS]
Referências encontradas : 200 [refinar]
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Id: biblio-1045757
Autor: Hou, G; Lu, J; Wang, H; Liu, Q; Tian, G; Yang, Y.
Título: Chemokine receptor 7 implications of spleen dendritic cells in multiple-organ dysfunction syndrome in mice / Implicaciones del receptor de la quimiocina de tipo 7 de las células dendríticas del bazo en el síndrome de disfunción orgánica múltiple en ratones
Fonte: West Indian med. j;62(9):787-792, Dec. 2013. ilus, graf.
Idioma: en.
Projeto: \"Eleventh Five\" Medical Research Project of PLA.
Resumo: OBJECTIVE: This study aims to explore the chemokine receptor 7 (CCR7) expression of spleen dendritic cells (DCs) and their role in the changes of migration and activity of spleen DCs in multiple-organ dysfunction syndrome (MODS). METHODS: The MODS model of mice was reproduced. The mice were randomly assigned to the following groups: normal, three-hour to six-hour, 24-hour to 48-hour, and 10-day to 12-day postzymosan injection. CD11c and CD205 were analysed by immunohistochemistry; the expressions of CD86 and CCR7 of DCs were studied using flow cytometry analyses. RESULTS: In normal mice, many DCs were found at the margin between the red and white pulp. In the three-hour to six-hour and 24- to 48-hour group, DC effectively upregulated CD86 and CCR7, and they were distributed in T-cell areas. In the 10-day to 12-day group, DCs were distributed at the margin by the immature form. CONCLUSION: The CCR7 expression level of DCs had close correlations with the migration of DCs. Chemokine receptor 7 can be used to evaluate the migration and functional activity of DCs in MODS.

OBJETIVO: Este estudio persigue explorar la expresión del receptor de la quimiocina 7 (CCR7) de células dendríticas del bazo (CD), y su papel en los cambios de la migración y la actividad del las células DC del bazo en el síndrome de disfunción orgánica múltiple (SDOM). MÉTODOS: Se reprodujo el modelo SDOM de los ratones. Los ratones fueron asignados aleatoriamente a los siguientes grupos de inyección de post-zymosan: hora normal, tres a seis horas, 24 horas a 48 horas, y de 10 a 12 días. CD11c y CD205 fueron analizados mediante inmunohistoquímica. Las expresiones de CD86 y CCR7 de CD se estudiaron mediante análisis de citometría de flujo. RESULTADOS: En los ratones normales, muchas células CD fueron encontradas en el margen entre la pulpa roja y la blanca. En el grupo de tres a seis horas y el grupo de 24 a 48 horas, CD86y CCR7 fueron efectivamente sobre-regulados en CD, y distribuidos en las áreas de células T. En el grupo de 10 a 12 días, las CDs fueron distribuidas en el margen por la forma inmadura. CONCLUSIÓN: El nivel de expresión CCR7 de las CDs tuvo estrecha correlación con la migración de las CDs. El receptor de la quimiocina de tipo 7 puede utilizarse para evaluar la migración y la actividad funcional de las CDs en SDOM.
Descritores: Baço/citologia
Células Dendríticas/imunologia
Receptores de Quimiocinas/imunologia
Insuficiência de Múltiplos Órgãos/patologia
-Imuno-Histoquímica
Movimento Celular
Modelos Animais de Doenças
Camundongos Endogâmicos C57BL
Insuficiência de Múltiplos Órgãos/imunologia
Limites: Animais
Masculino
Camundongos
Responsável: BR1.1 - BIREME


  2 / 200 LILACS  
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Id: biblio-838973
Autor: Seo, Hyang-Hee; Kim, Sang Woo; Lee, Chang Youn; Lim, Kyu Hee; Lee, Jiyun; Choi, Eunhyun; Lim, Soyeon; Lee, Seahyoung; Hwang, Ki-Chul.
Título: A spleen tyrosine kinase inhibitor attenuates the proliferation and migration of vascular smooth muscle cells
Fonte: Biol. Res;50:1, 2017. tab, graf.
Idioma: en.
Projeto: Future Planning; . Future Planning.
Resumo: BACKGROUND: Pathologic vascular smooth muscle cell (VSMC) proliferation and migration after vascular injury promotes the development of occlusive vascular disease. Therefore, an effective chemical agent to suppress aberrant proliferation and migration of VSMCs can be a potential therapeutic modality for occlusive vascular disease such as atherosclerosis and restenosis. To find an anti-proliferative chemical agent for VSMCs, we screened an in-house small molecule library, and the selected small molecule was further validated for its anti-proliferative effect on VSMCs using multiple approaches, such as cell proliferation assays, wound healing assays, transwell migration assays, and ex vivo aortic ring assay. RESULTS: Among 43 initially screened small molecule inhibitors of kinases that have no known anti-proliferative effect on VSMCs, a spleen tyrosine kinase (Syk) inhibitor (BAY61-3606) showed significant anti-proliferative effect on VSMCs. Further experiments indicated that BAY61 attenuated the VSMC proliferation in both concentration- and time-dependent manner, and it also significantly suppressed the migration of VSMCs as assessed by both wound healing assays and transwell assays. Additionally, BAY61 suppressed the sprouting of VSMCs from endothelium-removed aortic rings. CONCLUSION: The present study identified a Syk kinase inhibitor as a potent VSMC proliferation and migration inhibitor and warrants further studies to elucidate its underlying molecular mechanisms, such as its primary target, and to validate its in vivo efficacy as a therapeutic agent for restenosis and atherosclerosis.
Descritores: Pirimidinas/farmacologia
Movimento Celular/efeitos dos fármacos
Niacinamida/análogos & derivados
Miócitos de Músculo Liso/efeitos dos fármacos
Proliferação de Células/efeitos dos fármacos
Quinase Syk/antagonistas & inibidores
Músculo Liso Vascular/efeitos dos fármacos
-Aorta Torácica/efeitos dos fármacos
Fatores de Tempo
Cicatrização/efeitos dos fármacos
Células Cultivadas
Western Blotting
Reprodutibilidade dos Testes
Ratos Sprague-Dawley
Niacinamida/farmacologia
Relação Dose-Resposta a Droga
Avaliação Pré-Clínica de Medicamentos
Ensaios de Migração Celular
Músculo Liso Vascular/citologia
Limites: Animais
Ratos
Tipo de Publ: Estudo de Avaliação
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-1012314
Autor: Zhang, Caixiang; Wang, Wenying; Lin, Jun; Xiao, Jing; Tian, Ye.
Título: lncRNA CCAT1 promotes bladder cancer cell proliferation, migration and invasion
Fonte: Int. braz. j. urol;45(3):549-559, May-June 2019. tab, graf.
Idioma: en.
Projeto: Beijing Municipal Administration of Hospitals Clinical Medicine Development of Special Funding.
Resumo: ABSTRACT Objective: To study the expression patterns of long noncoding RNA (lncRNA) colon cancer-associated transcript 1 (CCAT1) and the changes in cell proliferation, apoptosis, migration and invasion induced by silencing CCAT1 in bladder cancer cells. Materials and Methods: The expression levels of CCAT1 were determined using realtime quantitative polymerase chain reaction in cancerous tissues and paired normal tissues from 34 patients with bladder cancer. The relationship between clinical characteristics and CCAT1 expression was analyzed. And then we conducted cell experiments. Bladder urothelial carcinoma cell lines T24 and 5637 cells were transfected with CCAT1 small interfering RNA (siRNA) or scramble siRNA. Cell proliferation and apoptosis changes were determined using a Cell Counting Kit-8 (CCK-8) assay and a flow cytometry assay. Migration and invasion changes were measured using a wound healing assay and a trans-well assay. microRNAs (miRNAs) were predicted by Starbase 2.0, and their differential expression levels were studied. Results: CCAT1 was significantly upregulated in bladder cancer (P < 0.05). CCAT1 upregulation was positively related to tumor stage (P = 0.004), tumor grade (P = 0.001) and tumor size (P = 0.042). Cell proliferation, migration and invasion were promoted by abnormally expressed CCAT1. miRNAs miR-181b-5p, miR-152-3p, miR-24-3p, miR-148a-3p and miR-490-3p were potentially related to the aforementioned functions of CCAT1. Conclusion: CCAT1 plays an oncogenic role in urothelial carcinoma of the bladder. In addition, CCAT1 may be a potential therapeutic target in this cancer.
Descritores: Neoplasias da Bexiga Urinária/genética
Neoplasias da Bexiga Urinária/patologia
RNA Longo não Codificante/análise
-Sincalida/análise
Fatores de Tempo
Cicatrização/genética
Regulação para Baixo
Expressão Gênica
Regulação Neoplásica da Expressão Gênica
Regulação para Cima
Movimento Celular/genética
MicroRNAs/genética
RNA Interferente Pequeno
Linhagem Celular Tumoral
Proliferação de Células/genética
Reação em Cadeia da Polimerase em Tempo Real
Citometria de Fluxo
Limites: Humanos
Masculino
Feminino
Idoso
Responsável: BR1.1 - BIREME


  4 / 200 LILACS  
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Id: biblio-1134248
Autor: Lei, Haiming; Ma, Fujun; Jia, Renfeng; Tan, Bo.
Título: Effects of Arf6 downregulation on biological characteristics of human prostate cancer cells
Fonte: Int. braz. j. urol;46(6):950-961, Nov.-Dec. 2020. graf.
Idioma: en.
Resumo: ABSTRACT Objective To evaluate the effects of Arf6 downregulation on human prostate cancer cells. Materials and Methods The effects of Arf6 downregulation on cell proliferation, migration, invasion and apoptosis were assessed by MTT, BrdU, scratch, Transwell assays and flow cytometry respectively. AKT, p-AKT, ERK1/2, p-ERK1/2 and Rac1 protein expressions were detected by Western blot. Results Downregulating Arf6 by siRNA interference suppressed the mRNA and protein expressions of Arf6. The proliferation capacities of siRNA group at 48h, 72h, and 96h were significantly lower than those of control group (P <0.05). The migration distance of siRNA group at 18h was significantly shorter than that of control group (P <0.01). The number of cells penetrating Transwell chamber membrane significantly decreased in siRNA group compared with that of control group (P <0.01). After 24h, negative control and normal control groups had similar apoptotic rates (P >0.05) which were both significantly lower than that of siRNA group (P <0.01). After Arf6 expression was downregulated, p-ERK1/2 and Rac1 protein expressions were significantly lower than those of control group (P <0.05). Conclusion Downregulating Arf6 expression can inhibit the proliferation, migration and invasion of prostate cancer cells in vitro, which may be related to ERK1/2 phosphorylation and Rac1 downregulation.
Descritores: Neoplasias da Próstata/genética
-Regulação para Baixo
Regulação Neoplásica da Expressão Gênica
Movimento Celular
Apoptose
RNA Interferente Pequeno/genética
Linhagem Celular Tumoral
Proliferação de Células
Invasividade Neoplásica
Limites: Humanos
Masculino
Responsável: BR1.1 - BIREME


  5 / 200 LILACS  
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Id: biblio-950754
Autor: Ortiz, Gustavo; Salica, Juan P; Chuluyan, Eduardo H; Gallo, Juan E.
Título: Diabetic retinopathy: could the alpha-1 antitrypsin be a therapeutic option?
Fonte: Biol. Res;47:1-9, 2014. ilus, tab.
Idioma: en.
Resumo: Diabetic retinopathy is one of the most important causes of blindness. The underlying mechanisms of this disease include inflammatory changes and remodeling processes of the extracellular-matrix (ECM) leading to pericyte and vascular endothelial cell damage that affects the retinal circulation. In turn, this causes hypoxia leading to release of vascular endothelial growth factor (VEGF) to induce the angiogenesis process. Alpha-1 antitrypsin (AAT) is the most important circulating inhibitor of serine proteases (SERPIN). Its targets include elastase, plasmin, thrombin, trypsin, chymotrypsin, proteinase 3 (PR-3) and plasminogen activator (PAI). AAT modulates the effect of protease-activated receptors (PARs) during inflammatory responses. Plasma levels of AAT can increase 4-fold during acute inflammation then is so-called acute phase protein (APPs). Individuals with low serum levels of AAT could develop disease in lung, liver and pancreas. AAT is involved in extracellular matrix remodeling and inflammation, particularly migration and chemotaxis of neutrophils. It can also suppress nitric oxide (NO) by nitric oxide sintase (NOS) inhibition. AAT binds their targets in an irreversible way resulting in product degradation. The aim of this review is to focus on the points of contact between multiple factors involved in diabetic retinopathy and AAT resembling pleiotropic effects that might be beneficial.
Descritores: Inibidores de Serino Proteinase/uso terapêutico
alfa 1-Antitripsina/uso terapêutico
Retinopatia Diabética/tratamento farmacológico
-Hipóxia Celular
Inibidores de Serino Proteinase/metabolismo
Movimento Celular/fisiologia
Quimiotaxia/fisiologia
alfa 1-Antitripsina/metabolismo
NF-kappa B/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
Mediadores da Inflamação/antagonistas & inibidores
Óxido Nítrico Sintase/antagonistas & inibidores
Substâncias Protetoras/metabolismo
Receptores Ativados por Proteinase/metabolismo
Retinopatia Diabética/fisiopatologia
Radicais Livres
Inflamação/metabolismo
Anti-Inflamatórios/metabolismo
Anti-Inflamatórios/uso terapêutico
Neutrófilos/fisiologia
Limites: Humanos
Animais
Tipo de Publ: Revisão
Responsável: CL1.1 - Biblioteca Central


  6 / 200 LILACS  
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Id: biblio-950766
Autor: Doan, Chung Chinh; Le, Long Thanh; Hoang, Son Nghia; Do, Si Minh; Van Le, Dong.
Título: Simultaneous silencing of VEGF and KSP by siRNA cocktail inhibits proliferation and induces apoptosis of hepatocellular carcinoma Hep3B cells
Fonte: Biol. Res;47:1-15, 2014. ilus, graf, tab.
Idioma: en.
Resumo: BACKGROUND: Vascular endothelial growth factor (VEGF) is involved in the growth of new blood vessels that feed tumors and kinesin spindle protein (KSP) plays a critical role in mitosis involving in cell proliferation. Simultaneous silencing of VEGF and KSP, an attractive and viable approach in cancer, leads on restricting cancer progression. The purpose of this study is to examine the therapeutic potential of dual gene targeted siRNA cocktail on human hepatocellular carcinoma Hep3B cells. RESULTS: The predesigned siRNAs could inhibit VEGF and KSP at mRNA level. siRNA cocktail showed a further downregulation on KSP mRNA and protein levels compared to KSP-siRNA or VEGF-siRNA, but not on VEGF expression. It also exhibited greater suppression on cell proliferation as well as cell migration or invasion capabilities and induction of apoptosis in Hep3B cells than single siRNA simultaneously. This could be explained by the significant downregulation of Cyclin D1, Bcl-2 and Survivin. However, no sigificant difference in the mRNA and protein levels of ANG2, involving inhibition of angiogenesis was found in HUVECs cultured with supernatant of Hep3B cells treated with siRNA cocktail, compared to that of VEGF-siRNA. CONCLUSION: Silencing of VEGF and KSP plays a key role in inhibiting cell proliferation, migration, invasion and inducing apoptosis of Hep3B cells. Simultaneous silencing of VEGF and KSP using siRNA cocktail yields promising results for eradicating hepatocellular carcinoma cells, a new direction for liver cancer treatment.
Descritores: Cinesina/genética
Apoptose/genética
Inativação Gênica
RNA Interferente Pequeno/genética
Fator A de Crescimento do Endotélio Vascular/genética
Proliferação de Células/genética
-Sais de Tetrazólio
Transfecção
Inibidores de Cisteína Proteinase/metabolismo
Regulação para Baixo
Movimento Celular
Western Blotting
Cinesina/metabolismo
Anexina A5
Genes bcl-2
Ciclina D1/metabolismo
Proteínas de Transporte Vesicular/metabolismo
Linhagem Celular Tumoral
Fator A de Crescimento do Endotélio Vascular/metabolismo
Proteínas Inibidoras de Apoptose/metabolismo
Células Endoteliais da Veia Umbilical Humana/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Citometria de Fluxo
Survivina
Mitose/genética
Limites: Humanos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: CL1.1 - Biblioteca Central


  7 / 200 LILACS  
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Id: biblio-1057503
Autor: Hou, Jian; Yue, Yuan; Hu, Bo; Xu, Guangtao; Su, Ruibing; Lv, Linhua; Huang, Jiaxing; Yao, Jianping; Guan, Yuanjun; Wang, Keke; Wu, Zhongkai.
Título: Dact1 involvement in the cytoskeletal arrangement of cardiomyocytes in atrial fibrillation by regulating cx43
Fonte: Rev. bras. cir. cardiovasc = Braz. j. cardiovasc. surg. (impr.);34(6):711-722, Nov.-Dec. 2019. tab, graf.
Idioma: en.
Projeto: National Key R&D Program of China; . the National Natural Science Foundation of China; . the Sci-Tech Planning Project of Zhejiang Province.
Resumo: Abstract Objective: To determine the role of the dishevelled binding antagonist of beta catenin 1 (DACT1) in the cytoskeletal arrangement of cardiomyocytes in atrial fibrillation (AF). Methods: The DACT1 expression and its associations with the degree of fibrosis and β-catenin in valvular disease patients were analyzed by immunohistochemistry and Masson's staining. DACT1 was overexpressed in the atrial myocyte cell line (HL-1) and the cardiac cell line (H9C2) by adenoviral vectors. Alterations in the fibrous actin (F-actin) content and organization and the expression of β-catenin were detected by flow cytometry, immunofluorescence, and Western blotting. Additionally, the association of DACT1 with gap junctions connexin 43 (Cx43) was detected by immunohistochemistry, immunofluorescence, and Western blotting. Results: Decreased cytoplasmic DACT1 expression in the myocardium was associated with AF (P=0.037) and a high degree of fibrosis (weak vs. strong, P=0.028; weak vs. very strong, P=0.029). A positive association was observed between DACT1 and β-catenin expression in clinical samples (P=0.028, Spearman's rho=0.408). Furthermore, overexpression of DACT1 in HL-1 and H9C2 cells induced an increase in β-catenin and subsequent partial colocalization of DACT1 and β-catenin. In addition, F-actin content and organization were enhanced. Interestingly, DACT1 was positively correlated with the Cx43 expression in clinical samples (P=0.048, Spearman's rho=0.370) and changed the Cx43 distribution in cardiac cell lines. Conclusion: DACT1 proved to be a novel AF-related gene by regulating Cx43 via cytoskeletal organization induced by β-catenin accumulation in cardiomyocytes. DACT1 could thus serve as a potential therapeutic marker for AF.
Descritores: Fibrilação Atrial/metabolismo
Citoesqueleto/metabolismo
Proteínas Nucleares/metabolismo
Conexina 43/metabolismo
Miócitos Cardíacos/citologia
Proteínas Adaptadoras de Transdução de Sinal/metabolismo
-Fibrilação Atrial/fisiopatologia
Fibrilação Atrial/genética
Imuno-Histoquímica
Proteínas Nucleares/genética
Movimento Celular
Conexina 43/genética
Proteínas Adaptadoras de Transdução de Sinal/genética
Limites: Humanos
Masculino
Feminino
Adulto
Pessoa de Meia-Idade
Idoso
Adulto Jovem
Responsável: BR1.1 - BIREME


  8 / 200 LILACS  
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Id: biblio-950801
Autor: Cai, Guilan; Qiao, Shanshan; Chen, Kui.
Título: Suppression of miR-221 inhibits glioma cells proliferation and invasion via targeting SEMA3B
Fonte: Biol. Res;48:1-8, 2015. ilus, graf.
Idioma: en.
Resumo: BACKGROUND: Gliomas are the most common primary tumors in the central nervous system. Due to complicated signaling pathways involved in glioma progression, effective targets for treatment and biomarkers for prognosis prediction are still scant. RESULTS: In this study we revealed that a new microRNA (miR), the miR-221, was highly expressed in the glioma cells, and suppression of miR-221 resulted in decreased cellular proliferation, migration, and invasion in glioma cells. Mechanistic experiments validated that miR-221 participates in regulating glioma cells proliferation and invasion via suppression of a direct target gene, the Semaphorin 3B (SEMA3B). The rescue experiment with miR-221 and SEMA3B both knockdown results in significant reversion of miR-221 induced phenotypes. CONCLUSION: Taken together, our findings highlight an unappreciated role for miR-221 and SEMA3B in glioma.
Descritores: Neoplasias Encefálicas/patologia
Glicoproteínas de Membrana/farmacologia
Apoptose
Semaforinas/farmacologia
MicroRNAs/antagonistas & inibidores
Proliferação de Células
Glioma/patologia
-Neoplasias Encefálicas/metabolismo
Glicoproteínas de Membrana/genética
Transdução de Sinais
Regulação Neoplásica da Expressão Gênica
Movimento Celular
Western Blotting
Semaforinas/genética
MicroRNAs/metabolismo
Linhagem Celular Tumoral
Reação em Cadeia da Polimerase em Tempo Real
Glioma/metabolismo
Luciferases/metabolismo
Invasividade Neoplásica
Limites: Humanos
Responsável: CL1.1 - Biblioteca Central


  9 / 200 LILACS  
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Id: biblio-950809
Autor: Lee, Seahyoung; Yun, Ina; Ham, Onju; Lee, Se-Yeon; Lee, Chang Yeon; Park, Jun-Hee; Lee, Jiyun; Seo, Hyang-Hee; Choi, Eunhyun; Hwang, Ki-Chul.
Título: Suppression of miR-181 a attenuates H2O2-induced death of mesenchymal stem cells by maintaining hexokinase II expression
Fonte: Biol. Res;48:1-7, 2015. graf.
Idioma: en.
Projeto: Korea Science and Engineering Foundation; . Ministry of Health and Welfare. Grant from the Korea Health 21 R&´D Project.
Resumo: BACKGROUND: Low survival rate of transplanted cells compromises the efficacy of cell therapy. Hexokinase II (HKII) is known to have anti-apoptotic activity through its interaction with mitochondria. The objective was to identify miRNAs targeting HKII and investigate whether miRNA-mediated modulation of HKII could improve the survival of mesenchymal stem cells (MSCs) exposed to H2O2. The expression of HKII in MSCs exposed to H2O2 was evaluated, and HKII-targeting miRNA was screened based on miRNA-target prediction databases. The effect of H2O2 on the expression of the selected HKII-targeting miRNA was examined and the effect of modulation of the selected HKII-targeting miRNA using anti-miRNA on H2O2-induced apoptosis of MSC was evaluated. RESULTS: H2O2 (600 µM) induced cell death of MSCs and decreased mitochondrial HKII expression. We have identified miR-181a as a HKII-targeting miRNA and H2O2 increased the expression of miR-181a in MSCs. Delivery of anti-miR-181a, which neutralizes endogenous miR-181a, significantly attenuated H2O2-induced decrease of HKII expression and disruption of mitochondrial membrane potential, improving the survival of MSCs exposed to H2O2. CONCLUSIONS: These findings suggest that H2O2-induced up-regulation of miR-181a contributes to the cell death of MSCs by down-regulating HKII. Neutralizing miR-181a can be an effective way to prime MSCs for transplantation into ischemic tissues.
Descritores: Apoptose
MicroRNAs/metabolismo
Células-Tronco Mesenquimais/patologia
Glioma/patologia
Hexoquinase/metabolismo
Peróxido de Hidrogênio/toxicidade
-Glicoproteínas de Membrana/genética
Glicoproteínas de Membrana/metabolismo
Diferenciação Celular
Movimento Celular
Sobrevivência Celular
Espécies Reativas de Oxigênio
Semaforinas/genética
Semaforinas/metabolismo
MicroRNAs/antagonistas & inibidores
Células-Tronco Mesenquimais/efeitos dos fármacos
Células-Tronco Mesenquimais/enzimologia
Reação em Cadeia da Polimerase em Tempo Real
Glioma/metabolismo
Peróxido de Hidrogênio/administração & dosagem
Mitocôndrias/enzimologia
Invasividade Neoplásica
Limites: Humanos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: CL1.1 - Biblioteca Central


  10 / 200 LILACS  
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Id: biblio-950812
Autor: Mikami, Taro; Yoshida, Keiichiro; Sawada, Hajime; Esaki, Michiyo; Yasumura, Kazunori; Ono, Michio.
Título: Inhibition of Rho-associated kinases disturbs the collective cell migration of stratified TE-10 cells
Fonte: Biol. Res;48:1-15, 2015. ilus, graf, tab.
Idioma: en.
Resumo: BACKGROUND: The collective cell migration of stratified epithelial cells is considered to be an important phenomenon in wound healing, development, and cancer invasion; however, little is known about the mechanisms involved. Furthermore, whereas Rho family proteins, including RhoA, play important roles in cell migration, the exact role of Rho-associated coiled coil-containing protein kinases (ROCKs) in cell migration is controversial and might be cell-type dependent. Here, we report the development of a novel modified scratch assay that was used to observe the collective cell migration of stratified TE-10 cells derived from a human esophageal cancer specimen. RESULTS: Desmosomes were found between the TE-10 cells and microvilli of the surface of the cell sheet. The leading edge of cells in the cell sheet formed a simple layer and moved forward regularly; these rows were followed by the stratified epithelium. ROCK inhibitors and ROCK small interfering RNAs (siRNAs) disturbed not only the collective migration of the leading edge of this cell sheet, but also the stratified layer in the rear. In contrast, RhoA siRNA treatment resulted in more rapid migration of the leading rows and disturbed movement of the stratified portion. CONCLUSIONS: The data presented in this study suggest that ROCKs play an important role in mediating the collective migration of TE-10 cell sheets. In addition, differences between the effects of siRNAs targeting either RhoA or ROCKs suggested that distinct mechanisms regulate the collective cell migration in the simple epithelium of the wound edge versus the stratified layer of the epithelium.
Descritores: Movimento Celular/fisiologia
RNA Interferente Pequeno/farmacologia
Quinases Associadas a rho/fisiologia
-Neoplasias Esofágicas
MicroRNAs/fisiologia
Linhagem Celular Tumoral
Quinases Associadas a rho/antagonistas & inibidores
Limites: Humanos
Responsável: CL1.1 - Biblioteca Central



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