Base de dados : LILACS
Pesquisa : E05.393.350.810 [Categoria DeCS]
Referências encontradas : 127 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 13 ir para página                         

  1 / 127 LILACS  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Brasil
Texto completo
Id: biblio-1101099
Autor: Muler, Mari Luminosa; Antunes, Fernanda; Guarache, Gabriel Cicolin; Oliveira, Rafaela Brito; Ureshino, Rodrigo Portes; Bincoletto, Claudia; Pereira, Gustavo José da Silva; Smaili, Soraya Soubhi.
Título: Effects of ICI 182, 780, an ERα and ERß antagonist, and G-1, a GPER agonist, on autophagy in breast cancer cells / Efeitos do antagonista seletivo do REα e do REß ICI 182, 780 e do agonista de GPER G-1 no processo de autofagia em células de câncer de mama
Fonte: Einstein (Säo Paulo);18:eAO4560, 2020. graf.
Idioma: en.
Projeto: Fundação de Amparo à Pesquisa do Estado de São Paulo; . Fundação de Amparo à Pesquisa do Estado de São Paulo; . Fundação de Amparo à Pesquisa do Estado de São Paulo.
Resumo: ABSTRACT Objective To investigate if ICI 182,780 (fulvestrant), a selective estrogen receptor alpha/beta (ERα/ERβ) antagonist, and G-1, a selective G-protein-coupled receptor (GPER) agonist, can potentially induce autophagy in breast cancer cell lines MCF-7 and SKBr3, and how G-1 affects cell viability. Methods Cell viability in MCF-7 and SKBr3 cells was assessed by the MTT assay. To investigate the autophagy flux, MCF-7 cells were transfected with GFP-LC3, a marker of autophagosomes, and analyzed by real-time fluorescence microscopy. MCF-7 and SKBr3 cells were incubated with acridine orange for staining of acidic vesicular organelles and analyzed by flow cytometry as an indicator of autophagy. Results Regarding cell viability in MCF-7 cells, ICI 182,780 and rapamycin, after 48 hours, led to decreased cell proliferation whereas G-1 did not change viability over the same period. The data showed that neither ICI 182,780 nor G-1 led to increased GFP-LC3 puncta in MCF-7 cells over the 4-hour observation period. The cytometry assay showed that ICI 182,780 led to a higher number of acidic vesicular organelles in MCF-7 cells. G-1, in turn, did not have this effect in any of the cell lines. In contrast, ICI 182,780 and G-1 did not decrease cell viability of SKBr3 cells or induce formation of acidic vesicular organelles, which corresponds to the final step of the autophagy process in this cell line. Conclusion The effect of ICI 182,780 on increasing acidic vesicular organelles in estrogen receptor-positive breast cancer cells appears to be associated with its inhibitory effect on estrogen receptors, and GPER does notseem to be involved. Understanding these mechanisms may guide further investigations of these receptors' involvement in cellular processes of breast cancer resistance.

RESUMO Objetivo Avaliar o efeito dos compostos ICI 182,780 (fulvestranto), um antagonista seletivo dos receptores de estrógeno alfa/beta (REα/REβ), e do G-1, um agonista seletivo de receptores de estrógeno acoplados a proteínas-G (GPER), na possível indução de autofagia em linhagens de câncer de mama MCF-7 e SKBr3, bem como o efeito de G-1 na viabilidade celular. Métodos A viabilidade celular de células MCF-7 e SKBr3 foi avaliada pelo ensaio com MTT. Para investigar a indução da autofagia, células MCF-7 foram transfectadas com GFP-LC3, um marcador de autofagossomos, e analisadas por microscopia de fluorescência em tempo real. As células MCF-7 e SKBr3 foram incubadas com o indicador de compartimentos ácidos laranja de acridina e analisadas por citometria de fluxo como indicativo para autofagia. Resultados Em células MCF-7, o ICI 182,780 e rapamicina após 48 horas levaram à diminuição da viabilidade celular, enquanto o G-1 não alterou a viabilidade no mesmo período de tratamento. Nem o ICI 182,780 e nem o G-1 induziram aumento na pontuação de GFP-LC3 em células MCF-7 até 4 horas. Já os ensaios de citometria de fluxo demonstraram que ICI 182,780 levou ao aumento de compartimentos ácidos em células MCF-7. O G-1 não aumentou estes parâmetros em ambas as linhagens. Por outro lado, ICI 182,780 e G-1 não induziram à redução da viabilidade em células SKBr3 e nem à formação de compartimentos ácidos, como etapa final do processo autofágico. Conclusão O aumento de compartimentos ácidos pelo ICI 182,780 em células de câncer de mama positivas para receptores de estrógeno parece estar associado com seu efeito inibidor de receptores de estrógeno, mas sem o envolvimento de GPER. A compreensão desses mecanismos pode direcionar estudos sobre o envolvimento dos receptores nos processos celulares de resistência do câncer de mama.
Descritores: Autofagia/efeitos dos fármacos
Neoplasias da Mama/patologia
Neoplasias da Mama/tratamento farmacológico
Receptores Acoplados a Proteínas G/agonistas
Antagonistas do Receptor de Estrogênio/farmacologia
Fulvestranto/farmacologia
-Fatores de Tempo
Transfecção/métodos
Sobrevivência Celular/efeitos dos fármacos
Western Blotting
Reprodutibilidade dos Testes
Análise de Variância
Sirolimo/farmacologia
Receptores Acoplados a Proteínas G/análise
Receptor alfa de Estrogênio/antagonistas & inibidores
Receptor beta de Estrogênio/antagonistas & inibidores
Proliferação de Células/efeitos dos fármacos
Células MCF-7
Citometria de Fluxo/métodos
Limites: Humanos
Feminino
Tipo de Publ: Estudo de Avaliação
Responsável: BR1.1 - BIREME


  2 / 127 LILACS  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Chile
Texto completo
Id: biblio-838963
Autor: Kong, Yanping; Zhang, Xianbo; Zhao, Yongliang; Xue, Yanfang; Zhang, Ye.
Título: Uptake of DNA by cancer cells without a transfection reagent
Fonte: Biol. Res;50:2, 2017. graf.
Idioma: en.
Projeto: Hebei province.
Resumo: BACKGROUND: Cancer cells exhibit elevated levels of glucose uptake and may obtain pre-formed, diet-derived fatty acids from the bloodstream to boost their rapid growth; they may also use nucleic acid from their microenvironment. The study of processing nucleic acid by cancer cells will help improve the understanding of the metabolism of cancer. DNA is commonly packaged into a viral or lipid particle to be transferred into cells; this process is called transfection in laboratory. Cancer cells are known for having gene mutations and the evolving ability of endocytosis. Their uptake of DNAs might be different from normal cells; they may take in DNAs directly from the environment. In this report, we studied the uptake of DNAs in cancer cells without a transfection reagent. METHODS: A group of DNA fragments were prepared with PCR and labeled with isotope phosphorous-32 to test their uptake by Huh 7 (liver cancer) and THLE3 (normal liver cells) after incubation overnight by counting radioactivity of the cells' genomic DNA. Multiple cell lines including breast cancer and lung cancer were tested with the same method. DNA molecules were also labeled with fluorescence to test the location in the cells using a kit of "label it fluorescence in situ hybridization (FISH)" from Mirus (USA). RESULTS: The data demonstrated that hepatocellular carcinoma cells possess the ability to take in large DNA fragments directly without a transfection reagent whereas normal liver cells cannot. Huh7 and MDA-MB231 cells displayed a significantly higher Rhodamine density in the cytoplasmic phagosomes and this suggests that the mechanism of uptake of large DNA by cancer cells is likely endocytosis. The efficacy of uptake is related to the DNA's size. Some cell lines of lung cancer and breast cancer also showed similar uptake of DNA. CONCLUSIONS: In the present study, we have revealed the evidence that some cancer cells, but not nontumorigenic cells, can take DNA fragments directly from the environment without the aid of the transfecting reagent.
Descritores: DNA/metabolismo
Transfecção
Neoplasias/genética
-Neoplasias da Mama/genética
Neoplasias da Mama/patologia
alfa-Fetoproteínas/metabolismo
Linhagem Celular
Reação em Cadeia da Polimerase
Hibridização in Situ Fluorescente
Hepatócitos/metabolismo
Genômica
Linhagem Celular Tumoral
Endocitose/genética
Fragmentação do DNA
Lipídeos/farmacologia
Neoplasias Hepáticas/genética
Neoplasias Hepáticas/patologia
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/patologia
Neoplasias/patologia
Limites: Humanos
Feminino
Responsável: CL1.1 - Biblioteca Central


  3 / 127 LILACS  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Brasil
Texto completo
Id: biblio-1040072
Autor: Li, Xue-Chao; Huang, Chuan-Xi; Wu, Shi-Kui; Yu, Lan; Zhou, Guang-Jian; Chen, Li-Jun.
Título: Biological roles of filamin a in prostate cancer cells
Fonte: Int. braz. j. urol;45(5):916-924, Sept.-Dec. 2019. graf.
Idioma: en.
Projeto: National Key Research and Development Program of China.
Resumo: ABSTRACT Objective This study aims to investigate the association of filamin A with the function and morphology of prostate cancer (PCa) cells, and explore the role of filamin A in the development of PCa, in order to analyze its significance in the evolvement of PCa. Materials and Methods A stably transfected cell line, in which filamin A expression was suppressed by RNA interference, was first established. Then, the effects of the suppression of filamin A gene expression on the biological characteristics of human PCa LNCaP cells were observed through cell morphology, in vitro cell growth curve, soft agar cloning assay, and scratch test. Results A cell line model with a low expression of filamin A was successfully constructed on the basis of LNCaP cells. The morphology of cells transfected with plasmid pSilencer-filamin A was the following: Cells were loosely arranged, had less connection with each other, had fewer tentacles, and presented a fibrous look. The growth rate of LNCap cells was faster than cells transfected with plasmid pSilencer-filamin A (P <0.05). The clones of LNCap cells in the soft agar cloning assay was significantly fewer than that of cells stably transfected with plasmid pSilencer-filamin A (P <0.05). Cells stably transfected with plasmid pSilencer-filamin A presented with a stronger healing and migration ability compared to LNCap cells (healing rate was 32.2% and 12.1%, respectively; P <0.05). Conclusion The expression of the filamin A gene inhibited the malignant development of LNCap cells. Therefore, the filamin A gene may be a tumor suppressor gene.
Descritores: Neoplasias da Próstata/patologia
Filaminas/análise
Filaminas/fisiologia
-Plasmídeos
Neoplasias da Próstata/genética
Sais de Tetrazólio
Fatores de Tempo
Cicatrização/fisiologia
Transfecção/métodos
Células Cultivadas
Western Blotting
Colorimetria/métodos
Linhagem Celular Tumoral
Proliferação de Células
Filaminas/genética
Formazans
Limites: Humanos
Masculino
Responsável: BR1.1 - BIREME


  4 / 127 LILACS  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Chile
Texto completo
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


  5 / 127 LILACS  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Chile
Texto completo
Id: biblio-950789
Autor: Zeng, Qiangcheng; Guo, Yong; Liu, Yongming; Li, Ruixin; Zhang, Xinchang; Liu, Lu; Wang, Yang; Zhang, Xizheng; Zou, Xianqiong.
Título: Integrin-ß1, not integrin-ß5, mediates osteoblastic differentiation and ECM formation promoted by mechanical tensile strain
Fonte: Biol. Res;48:1-8, 2015. graf, tab.
Idioma: en.
Projeto: National Nature Science Foundation of China; . Science Foundation of Tianjin; . Shandong Provincial Key Laboratory of Functional Macromolecular Biophysics.
Resumo: BACKGROUND: Mechanical strain plays a great role in growth and differentiation of osteoblast. A previous study indicated that integrin-ß (ß1, ß5) mediated osteoblast proliferation promoted by mechanical tensile strain. However, the involvement of integrin-ß; in osteoblastic differentiation and extracellular matrix (ECM) formation induced by mechanical tensile strain, remains unclear. RESULTS: After transfection with integrin-ß1 siRNA or integrin-ß5 siRNA, mouse MC3T3-E1 preosteoblasts were cultured in cell culture dishes and stimulated with mechanical tensile strain of 2500 microstrain (µÎµ) at 0.5 Hz applied once a day for 1 h over 3 or 5 consecutive days. The cyclic tensile strain promoted osteoblastic differentiation of MC3T3-E1 cells. Transfection with integrin-ß1 siRNA attenuated the osteoblastic diffenentiation induced by the tensile strain. By contrast, transfection with integrin-ß5 siRNA had little effect on the osteoblastic differentiation induced by thestrain. At thesametime, theresultofECM formation promoted by the strain, was similar to the osteoblastic differentiation. CONCLUSION: Integrin-ß1 mediates osteoblast differentiation and osteoblastic ECM formation promoted by cyclic tensile strain, and integrin-ß5 is not involved in the osteoblasts response to the tensile strain.
Descritores: Osteoblastos/fisiologia
Resistência à Tração/fisiologia
Diferenciação Celular/fisiologia
Integrina beta1/fisiologia
Cadeias beta de Integrinas/fisiologia
Matriz Extracelular/fisiologia
-Estresse Mecânico
Transfecção
Linhagem Celular
Western Blotting
RNA Interferente Pequeno
Proliferação de Células/fisiologia
Reação em Cadeia da Polimerase em Tempo Real
Limites: Animais
Camundongos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: CL1.1 - Biblioteca Central


  6 / 127 LILACS  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Chile
Texto completo
Id: biblio-1114696
Autor: Degerli, Elif; Torun, Vildan; Cansaran-Duman, Demet.
Título: miR-185-5p response to usnic acid suppresses proliferation and regulating apoptosis in breast cancer cell by targeting Bcl2
Fonte: Biol. Res;53:19, 2020. graf.
Idioma: en.
Projeto: Ankara University Management of Scientific Research Projects.
Resumo: BACKGROUND: Breast cancer is the most common cancer types among women. Recent researches have focused on determining the efficiency of alternative molecules and miRNAs in breast cancer treatment. The AIMof this study was to determine the effect of usnic acid response-miR-185-5p on proliferation in the breast cancer cell and to determine its relationship with apoptosis pathway. METHODS: The cell proliferation and cell apoptosis rate were significantly increased following the ectopic expression of miR-185-5p in BT-474 cells. Furthermore, the results of cell cycle assay performed by flow cytometry revealed that the transfection with miR-185-5p induced G1/S phase arrest. The apoptosis-related genes expression analysis was performed by qRT-PCR and the direct target of miR-185-5p in BT-474 cells was identified by western blot and luciferase reporter assay. RESULTS: Our data showed that miR-185-5p can cause significant changes in apoptosis-related genes expression levels, suggesting that cell proliferation was suppressed by miR-185-5p via inducing apoptosis in breast cancer cells. According to western blot results, miR-185-5p lead to decrease BCL2 protein level in BT-474 cells and direct target of miR-185-5p was identified as BCL by luciferase reporter assay. CONCLUSION: This study revealed that miR-185-5p may be an effective agent in the treatment of breast cancer.
Descritores: Benzofuranos/metabolismo
Neoplasias da Mama/genética
Proteínas Proto-Oncogênicas c-bcl-2/genética
MicroRNAs/genética
-Neoplasias da Mama/metabolismo
Transfecção
Transdução de Sinais
Regulação para Baixo
Regulação Neoplásica da Expressão Gênica
Apoptose
Proteínas Proto-Oncogênicas c-bcl-2
Reação em Cadeia da Polimerase Via Transcriptase Reversa
MicroRNAs/metabolismo
Linhagem Celular Tumoral
Proliferação de Células
Limites: Humanos
Feminino
Responsável: CL1.1 - Biblioteca Central


  7 / 127 LILACS  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Chile
Texto completo
Id: biblio-1089072
Autor: Zhao, Jun; Geng, Lijiao; Chen, Yong; Wu, Chunfang.
Título: SNHG1 promotes MPP+-induced cytotoxicity by regulating PTEN/AKT/mTOR signaling pathway in SH-SY5Y cells via sponging miR-153-3p
Fonte: Biol. Res;53:01, 2020. graf.
Idioma: en.
Resumo: BACKGROUND: Long non-coding RNA small molecule RNA host gene 1 (SNHG1) was previously identified to be relevant with Parkinson's disease (PD) pathogenesis. This work aims to further elucidate the regulatory networks of SNHG1 involved in PD. Methods: 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-hydrochloride (MPTP)-induced mice and 1-methyl-4-phenylpyridinium (MPP+)-treated SH-SY5Y cells were respectively constructed as the in vivo and in vitro PD models. Expression levels of SNHG1 and miR-153-3p were detected by qRT-PCR. Protein expression levels of phosphate and tension homology deleted on chromosome ten (PTEN) were measured by western blotting assay. Cell viability and apoptosis were determined by MTT and flow cytometry assays. The interactions among SNHG1, miR-153-3p and PTEN were identified by luciferase reporter assay, RNA immunoprecipitation, and/or RNA pull-down analysis. RESULTS: Increased SNHG1 expression was found in midbrain of MPTP-induced PD mice and MPP+-treated SH-SY5Y cells. Overexpression of SNHG1 lowered viability and enhanced apoptosis in MPP+-treated SH-SY5Y cells. Moreover, SNHG1 acted as a molecular sponge to inhibit the expression of miR-153-3p. Furthermore, miR-153-3p-mediated suppression of MPP+-induced cytotoxicity was abated following SNHG1 up-regulation. Additionally, PTEN was identified as a direct target of miR-153-3p, and SNHG1 could serve as a competing endogenous RNA (ceRNA) of miR-153-3p to improve the expression of PTEN. Besides, enforced expression of PTEN displayed the similar functions as SNHG1 overexpression in regulating the viability and apoptosis of MPP+-treated SH-SY5Y cells. Finally, SNHG1 was found to activate PTEN/AKT/mTOR signaling pathway in SH-SY5Y cells by targeting miR-153-3p. CONCLUSION: SNHG1 aggravates MPP+-induced cellular toxicity in SH-SY5Y cells by regulating PTEN/AKT/mTOR signaling via sponging miR-153-3p, indicating the potential of SNHG1 as a promising therapeutic target for PD.
Descritores: Doença de Parkinson/metabolismo
1-Metil-4-fenilpiridínio/toxicidade
PTEN Fosfo-Hidrolase/metabolismo
Proteínas Proto-Oncogênicas c-akt/metabolismo
Serina-Treonina Quinases TOR/metabolismo
RNA Longo não Codificante/metabolismo
-Doença de Parkinson/genética
Transfecção
Transdução de Sinais
Células Cultivadas
Regulação da Expressão Gênica
Western Blotting
Apoptose
MicroRNAs
Modelos Animais de Doenças
Reação em Cadeia da Polimerase em Tempo Real
RNA Longo não Codificante/genética
Camundongos Endogâmicos C57BL
Limites: Animais
Masculino
Camundongos
Responsável: CL1.1 - Biblioteca Central


  8 / 127 LILACS  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Brasil
Texto completo
Id: biblio-896296
Autor: Cheng, Yi; Gao, Yang; Zhao, Lu; Gao, Shunqiang; Zhang, Guoqiang; Zhang, Yan.
Título: Knockout of p16INK4a promotes aggregative growth of dermal papilla cells
Fonte: Rev. Assoc. Med. Bras. (1992);63(10):883-889, Oct. 2017. tab, graf.
Idioma: en.
Resumo: Summary Objective: Dermal papilla cells (DPCs) are located in the hair follicles and play an important role in hair growth. These cells have the ability to induce hair follicle formation when they display aggregative behavior. DPCs derived from the androgenetic alopecia (AGA) area undergo premature senescence in vitro, associated with p16INK4a expression. The aim of the current study was to investigate the expression of p16INK4a in aggregative and non-aggregative DPCs and the effect of p16INK4a down-regulation in these cells by adenovirus-mediated RNA interference (RNAi). Method: DPCs were isolated and cultured from healthy human scalp. p16INK4a gene and protein were detected in aggregative and non-aggregative cells. Expression of p16INK4a in DPCs was silenced by infection with rAd5-CDKN1A-1p2shRNA. Cell fate was monitored after infection. The growth of cells was measured by MTT assay. Cell cycle was evaluated by flow cytometry (FCM). Results: DPCs were isolated by digestion and showed aggregative behavior for six passages. The expression of p16INK4a showed a clear upward trend in non-aggregative cells when compared with aggregative group. p16INK4a expression was silenced by rAd5-CDKN1A-1p2shRNA (p<0.05). The p16INK4a-silenced cells grew more rapidly and exhibited a trend towards aggregative growth. There was an increase in the proportion of cells in G1 phase, while those in S phase were reduced after p16INK4a gene silencing (p<0.05). Conclusion: Our results suggest that p16INK4a plays an important role in the premature senescence and aggregative behavior of DPCs. These observations can lead to novel therapeutic strategies for treatment of AGA.
Descritores: Couro Cabeludo/citologia
Folículo Piloso/citologia
Genes p16/fisiologia
-Valores de Referência
Fatores de Tempo
Imuno-Histoquímica
Transfecção
Agregação Celular/genética
Ciclo Celular/genética
Células Cultivadas
Senescência Celular/genética
Derme/citologia
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Proliferação de Células/genética
Alopecia/genética
Técnicas de Inativação de Genes/métodos
Citometria de Fluxo
Limites: Humanos
Masculino
Responsável: BR1.1 - BIREME


  9 / 127 LILACS  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Brasil
Texto completo
Id: biblio-1041054
Autor: Huang, Yayi; Zhou, Fang; Xiao, Yeda; Shen, Cheng; Liu, Kang; Zhao, Bo.
Título: TLR7 mediates increased vulnerability to ischemic acute kidney injury in diabetes
Fonte: Rev. Assoc. Med. Bras. (1992);65(8):1067-1073, Aug. 2019. graf.
Idioma: en.
Projeto: Hubei Province.
Resumo: SUMMARY OBJECTIVE Diabetes is a risk factor for acute kidney injury (AKI). However, its mechanism of pathogenesis has not been elucidated. The aim of the study was to investigate the role of inflammation and the toll-like receptor 7 (TLR7) in ischemic AKI for diabetes. METHODS A high glucose hypoxia-reoxygenation model of human renal tubular epithelial (HK-2) cells was used to generate AKI induced by ischemia-reperfusion in diabetes. The activity of cells was measured by CCK-8 assay and LDH activity. Inflammatory cytokines were assessed by ELISA. TLR7, MyD88, and NF-κB expressions were examined by western blotting. Apoptosis was evaluated by flow cytometry. RESULTS The high glucose group and low glucose group were subjected to hypoxia-reoxygenation. The low glucose group developed only mild cell damage, apoptosis, and inflammatory response. In contrast, an equivalent hypoxia-reoxygenation injury provoked severe cell damage, apoptosis, and inflammatory response in the high glucose group. Expression of TLR7 and its related proteins were measured in the high glucose group before and after hypoxia-reoxygenation. The high glucose group exhibited more significant increases in TLR7 expression following hypoxia-reoxygenation than the low glucose group. In addition, the expression of TLR7 and its related proteins after hypoxia-reoxygenation were higher in the high glucose group than in the low glucose group. Inhibition of TLR7 provides significant protection against ischemic injury in diabetes. CONCLUSION Our results suggest that diabetes increases the vulnerability to ischemia-induced renal injury. This increased vulnerability originates from a heightened inflammatory response involving the TLR7 signal transduction pathway.

RESUMO OBJETIVO O diabetes é um fator de risco para a lesão renal aguda (LRA). No entanto, seu mecanismo de patogênese não foi elucidado. O objetivo do estudo foi investigar o papel da inflamação e do receptor Toll-like 7 (TLR7) na LRA isquêmica no diabetes. MÉTODOS Um modelo de hipóxia-reoxigenação de células epiteliais tubulares renais humanas (HK-2) na presença de concentrações altas de glicose foi utilizado para gerar LRA induzida por isquemia-reperfusão em diabetes. A atividade das células foi medida pelo ensaio Cell Counting Kit-8 (CCK-8) e pela atividade da lactato desidrogenase (LDH). As citocinas inflamatórias foram avaliadas por ensaio imunoenzimático (Elisa). A expressão de TLR7, do fator de diferenciação mieloide 88 (MyD88) e do fator de transcrição nuclear-κB (NF-κB) foi examinada por Western blotting. A apoptose foi avaliada por citometria de fluxo. RESULTADOS Os grupos glicose alta e glicose baixa foram submetidos à hipóxia-reoxigenação. O grupo de baixa glicose desenvolveu apenas danos celulares ligeiros, apoptose e uma resposta inflamatória. Em contraste, no grupo de alta glicose, uma lesão equivalente de hipóxia-reoxigenação provocou danos celulares graves, apoptose e uma resposta inflamatória. A expressão de TLR7 e suas proteínas relacionadas foi medida no grupo de alta glicose antes e após a hipóxia-reoxigenação. O grupo de alta glicose exibiu maiores aumentos na expressão de TLR7 após hipóxia-reoxigenação do que o grupo de baixa glicose. Além disso, a expressão de TLR7 e suas proteínas relacionadas após a hipóxia-reoxigenação foi maior no grupo com alto nível de glicose do que no grupo com baixo nível de glicose. A inibição do TLR7 fornece proteção significativa contra a lesão isquêmica no diabetes. CONCLUSÃO Nossos resultados sugerem que o diabetes aumenta a vulnerabilidade à lesão renal induzida por isquemia. Essa vulnerabilidade acrescida tem por origem uma resposta inflamatória aumentada envolvendo a via de transdução de sinal do TLR7.
Descritores: Diabetes Mellitus/metabolismo
Receptor 7 Toll-Like/metabolismo
Injúria Renal Aguda/metabolismo
Isquemia/metabolismo
-Transfecção
Transdução de Sinais
Células Cultivadas
RNA Interferente Pequeno
Diabetes Mellitus/fisiopatologia
Receptor 7 Toll-Like/fisiologia
Injúria Renal Aguda/fisiopatologia
Citometria de Fluxo
Isquemia/fisiopatologia
Limites: Humanos
Responsável: BR1.1 - BIREME


  10 / 127 LILACS  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Chile
Texto completo
Id: biblio-950902
Autor: Liu, Ping; Yu, Junyan; Tian, Xiangyang; Chang, Jianlan; Zhang, Ying; Zhang, Rong; Zhang, Ningning; Huang, Ranxing; Li, Lulu; Qiao, Xianli; Guo, Hongliang.
Título: The effect of downregulation of Stathmin gene on biological behaviors of U373 and U87-MG glioblastoma cells
Fonte: Biol. Res;51:16, 2018. tab, graf.
Idioma: en.
Resumo: BACKGROUND: Stathmin as a critical protein involved in microtubule polymerization, is necessary for survival of cancer cells. However, extremely little is known about Stathmin in glioblastoma. So, this study was designed to elucidate the function of Stathmin gene in the tumorigenesis and progression of glioblastoma cells. METHOD: The lentiviral interference vector pLV3-si-Stathmin targeting Stathmin gene and the control vector pLV3-NC were established for the co-transfection of 293T cells together with the helper plasmids. Viral titer was determined via limiting dilution assay. Then pLV3-si-Stathmin and pLV3-NC were stably co-transfected into U373 and U87-MG glioblastoma cells. Expression levels of Stathmin protein in each group were determined by using Western Blot, and the proliferation and migration ability of the cells with downregulated Stathmin were evaluated through CCK8 assay and transwell invasion assay, respectively. Cell cycles and cell apoptosis were detected with flow cytometry. Finally, the effect of Stathmin in tumor formation was determined in nude mice. RESULT: DNA sequencing and viral titer assay indicated that the lentiviral interference vector was successfully established with a viral titer of 4 × 108 TU/ml. According to the results from Western Blotting, Stathmin protein expression level decreased significantly in the U373 and U87-MG cells after transfected with pLV3-si-Stathmin, respectively, compared with those transfected with pLV3-NC. In glioblastoma cells, the cell proliferation and migration were greatly inhibited after the downregulation of Stathmin protein. Flow cytometry showed that much more cells were arrested in G2/M phasein Stathmin downregulated group, compared with the non-transfection group and NC group. But Stathmin downregulation did not induce significant cell apoptosis. Tumor formation assay in nude mice showed that tumor formation was delayed after Stathmin downregulation, with a reduction in both tumor formation rate and tumor growth velocity. CONCLUSION: Stathmin downregulation affected the biological behaviors of U373 and U87-MG glioblastoma cells, inhibiting the proliferation and migration of tumor cells. Stathmin gene may serve as a potential target in gene therapy for glioblastoma.
Descritores: Regulação para Baixo/genética
Glioblastoma/metabolismo
Proliferação de Células/genética
Estatmina/genética
-Transfecção
Glioblastoma/genética
Glioblastoma/patologia
Linhagem Celular Tumoral
Estatmina/metabolismo
Vetores Genéticos
Limites: Animais
Camundongos
Responsável: CL1.1 - Biblioteca Central



página 1 de 13 ir para página                         
   


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