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1.
J. pediatr. (Rio J.) ; 91(2): 136-142, Mar-Apr/2015. tab
Artigo em Inglês | LILACS (Américas) | ID: lil-745939

RESUMO

OBJECTIVE: To assess the effect of Leisure-time physical activity (LTPA) on cardiometabolic risk by nutritional status in Mexican children and adolescents. METHODS: This was a cross-sectional study conducted with 1,309 participants aged between 5 and 17 years. Nutritional status was classified according to the BMI Z-score by age and gender. A previously validated questionnaire was used to evaluate LTPA; a cardiometabolic risk score was calculated. Multiple linear regression analysis was performed to assess the effect of LTPA on cardiometabolic risk. RESULTS: After adjusting for risk factors, mild LTPA were positively associated with cardiometabolic risk score (ßMildvsIntenseLTPA: 0.68; 95% CI: 0.18 to 1.18; pfortrend = 0.007). This association became stronger when estimated for overweight (ß MildvsIntenseLTPA: 1.24; 95% CI: 0.24 to 2.24; pfortrend = 0.015) and obese participants (ß MildvsIntenseLTPA: 1.02; 95% CI: 0.07 to 1.97; pfortrend= 0.045) CONCLUSION: Mild LTPA was positively associated with cardiometabolic risk in overweight and obese children and adolescents. Given the emerging childhood obesity epidemic in Mexico, these results may be useful in the design of strategies and programs to increase physical activity levels in order to achieve better health. .


OBJETIVO: Avaliar o efeito da prática de AFL sobre o risco cardiometabólico em crianças e adolescentes mexicanos de acordo com sua situação nutricional. MÉTODOS: Estudo transversal feito com 1.309 participantes de cinco a 17 anos. A situação nutricional foi classificada de acordo com o escore z de IMC por idade e sexo. Um questionário validado anteriormente foi usado para avaliar a AFL; foi calculado um escore de risco cardiometabólico. A análise de regressão linear múltipla foi feita para avaliar o efeito de AFL sobre o risco cardiometabólico. RESULTADOS: Após o ajuste de acordo com os fatores de risco, a AFL leve foi positivamente associada ao escore de risco cardiometabólico (ßAFLLevexIntensa: 0,68; IC 95%: 0,18 a 1,18; p paratendência = 0,007). Essa associação foi mais intensa quando estimada para participantes acima do peso (ßAFLLevexIntensa: 1,24; IC 95%: 0,24 a 2,24; p paratendência = 0,015) e obesos (ßAFLLevexIntensa: 1,02; IC 95%: 0,07 a 1,97; p paratendência = 0,045). CONCLUSÃO: A AFL leve foi positivamente associada ao escore de risco cardiometabólico em crianças e adolescentes acima do peso e obesos. Considerando a epidemia de obesidade infantil emergente no México, esses resultados poderão ser úteis na elaboração de estratégias e programas para aumentar os níveis de atividade física a fim de obter uma saúde melhor. .


Assuntos
Animais , Humanos , Camundongos , Proteína Axina/genética , Neoplasias Colorretais/genética , Proteínas de Ligação a DNA/genética , Fator 1 de Ligação ao Facilitador Linfoide/genética , Tanquirases/antagonistas & inibidores , Fatores de Transcrição/genética , beta Catenina/genética , Linhagem Celular , Linhagem Celular Tumoral , Transdução de Sinais/genética , Transcrição Genética/genética , Proteínas Wnt/genética
2.
Artigo em Inglês | WPRIM (Pacífico Ocidental) | ID: wprim-141161

RESUMO

The Wnt signaling pathway has regulatory roles in cell proliferation, differentiation, and polarity. Aberrant Wnt pathway regulation can lead to abnormal cell proliferation and cancer, and loss of Wnt7a expression has been demonstrated in lung cancer cell lines. E-cadherin keeps intercellular integrity and prevents metastasis. Therefore, E-cadherin has been known as a prognostic factor in cancer. In the present study, we investigated the E-cadherin expression status by immunohistochemical stain and the Wnt7a promoter methylation status in human non-small cell lung carcinoma (NSCLC) by methylation-specific PCR. We also analyzed their correlations with clinicopathological factors. Methylation of the Wnt7a gene promoter was detected in the lung tissues of 32 of 121 (26.4%) patients with NSCLC. Wnt7a promoter methylation was correlated with advanced tumor stage (P = 0.036) and distant metastasis (P = 0.037). In addition, Wnt7a promoter methylation showed correlation with loss of E-cadherin expression (P < 0.001). However, Wnt7a promoter methylation was not closely related with gender, age, histological type, or smoking habit. Even though Wnt7a methylation could not show significant correlation with the long term survival of the patients with limited follow up data, these findings suggest that loss of the Wnt7a gene induced by promoter methylation might be another prognostic factor for NSCLC and that restoration of Wnt7a may be a promising treatment for NSCLC.


Assuntos
Caderinas/biossíntese , Carcinoma Pulmonar de Células não Pequenas/genética , Metilação de DNA/genética , Feminino , Humanos , Neoplasias Pulmonares/genética , Masculino , Pessoa de Meia-Idade , Metástase Neoplásica/genética , Estadiamento de Neoplasias , Regiões Promotoras Genéticas/genética , República da Coreia , Biomarcadores Tumorais/genética , Proteínas Wnt/genética
3.
Artigo em Inglês | WPRIM (Pacífico Ocidental) | ID: wprim-141160

RESUMO

The Wnt signaling pathway has regulatory roles in cell proliferation, differentiation, and polarity. Aberrant Wnt pathway regulation can lead to abnormal cell proliferation and cancer, and loss of Wnt7a expression has been demonstrated in lung cancer cell lines. E-cadherin keeps intercellular integrity and prevents metastasis. Therefore, E-cadherin has been known as a prognostic factor in cancer. In the present study, we investigated the E-cadherin expression status by immunohistochemical stain and the Wnt7a promoter methylation status in human non-small cell lung carcinoma (NSCLC) by methylation-specific PCR. We also analyzed their correlations with clinicopathological factors. Methylation of the Wnt7a gene promoter was detected in the lung tissues of 32 of 121 (26.4%) patients with NSCLC. Wnt7a promoter methylation was correlated with advanced tumor stage (P = 0.036) and distant metastasis (P = 0.037). In addition, Wnt7a promoter methylation showed correlation with loss of E-cadherin expression (P < 0.001). However, Wnt7a promoter methylation was not closely related with gender, age, histological type, or smoking habit. Even though Wnt7a methylation could not show significant correlation with the long term survival of the patients with limited follow up data, these findings suggest that loss of the Wnt7a gene induced by promoter methylation might be another prognostic factor for NSCLC and that restoration of Wnt7a may be a promising treatment for NSCLC.


Assuntos
Caderinas/biossíntese , Carcinoma Pulmonar de Células não Pequenas/genética , Metilação de DNA/genética , Feminino , Humanos , Neoplasias Pulmonares/genética , Masculino , Pessoa de Meia-Idade , Metástase Neoplásica/genética , Estadiamento de Neoplasias , Regiões Promotoras Genéticas/genética , República da Coreia , Biomarcadores Tumorais/genética , Proteínas Wnt/genética
4.
Artigo em Inglês | WPRIM (Pacífico Ocidental) | ID: wprim-228161

RESUMO

Airway remodeling is a key characteristic of chronic asthma, particularly in patients with a fixed airflow limitation. The mechanisms underlying airway remodeling are poorly understood, and no therapeutic option is available. The Wnt/beta-catenin signaling pathway is involved in various physiological and pathological processes, including fibrosis and smooth muscle hypertrophy. In this study, we investigated the roles of Wnt/beta-catenin signaling in airway remodeling in patients with asthma. Wnt7a mRNA expression was prominent in induced sputum from patients with asthma compared with that from healthy controls. Next, we induced a chronic asthma mouse model with airway remodeling features, including subepithelial fibrosis and airway smooth muscle hyperplasia. Higher expression of Wnt family proteins and beta-catenin was detected in the lung tissue of mice with chronic asthma compared to control mice. Blocking beta-catenin expression with a specific siRNA attenuated airway inflammation and airway remodeling. Decreased subepithelial fibrosis and collagen accumulation in the beta-catenin siRNA-treated mice was accompanied by reduced expression of transforming growth factor-beta. We further showed that suppressing beta-catenin in the chronic asthma model inhibited smooth muscle hyperplasia by downregulating the tenascin C/platelet-derived growth factor receptor pathway. Taken together, these findings demonstrate that the Wnt/beta-catenin signaling pathway is highly expressed and regulates the development of airway remodeling in chronic asthma.


Assuntos
Adulto , Idoso , Remodelação das Vias Aéreas , Animais , Asma/genética , Doença Crônica , Feminino , Fibrose , Regulação da Expressão Gênica , Humanos , Pulmão/metabolismo , Masculino , Camundongos Endogâmicos BALB C , Pessoa de Meia-Idade , Interferência de RNA , RNA Mensageiro/genética , RNA Interferente Pequeno/genética , Proteínas Wnt/genética , Via de Sinalização Wnt , beta Catenina/genética
5.
Clinics ; 66(11): 1849-1854, 2011. ilus, tab
Artigo em Inglês | LILACS (Américas) | ID: lil-605862

RESUMO

INTRODUCTION: Activating mutations in exon 3 of the β-catenin gene are involved in the pathogenesis of adamantinomatous craniopharyngiomas. Recently, the interaction between β-catenin and PROP1 has been shown to be responsible for pituitary cell lineage determination. We hypothesized that dysregulated PROP1 expression could also be involved in the pathogenesis of craniopharyngiomas OBJECTIVES: To determine whether dysregulated gene expression was responsible for tumor pathogenesis in adamantinomatous craniopharyngiomas, the β-catenin gene was screened for mutations, and the expression of the β-catenin gene and PROP1 was evaluated. β-catenin gene was amplified and sequenced from 14 samples of adamantinomatous craniopharyngiomas. PROP1 and β-catenin gene expression was assessed by real-time RT-PCR from 12 samples, and β-catenin immunohistochemistry was performed on 11 samples. RESULTS: Mutations in the β-catenin gene were identified in 64 percent of the adamantinomatous craniopharyngiomas samples. Evidence of β-catenin gene overexpression was found in 71 percent of the tumors with β-catenin mutations and in 40 percent of the tumors without mutations, and β-catenin immunohistochemistry revealed a nuclear staining pattern for each of the analyzed samples. PROP1 expression was undetectable in all of the tumor samples. CONCLUSION: We found evidence of β-catenin gene overexpression in the majority of adamantinomatous craniopharyngiomas, and we also detected a nuclear β-catenin staining pattern regardless of the presence of a bcatenin gene mutation. These results suggest that WNT signaling activation plays an important role in the pathogenesis of adamantinomatous craniopharyngiomas. Additionally, this study was the first to evaluate PROP1 expression in adamantinomatous craniopharyngiomas, and the absence of PROP1 expression indicates that this gene is not involved in the pathogenesis of this tumor, at least in this cohort.


Assuntos
Adolescente , Criança , Pré-Escolar , Feminino , Humanos , Lactente , Masculino , Adulto Jovem , Craniofaringioma/genética , Proteínas de Homeodomínio/genética , Neoplasias Hipofisárias/genética , beta Catenina/genética , Craniofaringioma/patologia , Análise Mutacional de DNA , Expressão Gênica , Neoplasias Hipofisárias/patologia , Transdução de Sinais/genética , Ativação Transcricional/genética , Proteínas Wnt/genética
6.
Artigo em Inglês | WPRIM (Pacífico Ocidental) | ID: wprim-71513

RESUMO

Wnt signaling is known to be important for diverse embryonic and post-natal cellular events and be regulated by the proteins Dishevelled and Axin. Although Dishevelled is activated by Wnt and involved in signal transduction, it is not clear how Dishevelled-mediated signaling is turned off. We report that guanine nucleotide binding protein beta 2 (Gnb2; Gbeta2) bound to Axin and Gbeta2 inhibited Wnt mediated reporter activity. The inhibition involved reduction of the level of Dishevelled, and the Gbeta2gamma2 mediated reduction of Dishevelled was countered by increased expression of Axin. Consistent with these effects in HEK293T cells, injection of Gbeta2gamma2 into Xenopus embryos inhibited the formation of secondary axes induced either by XWnt8 or Dishevelled, but not by beta-catenin. The DEP domain of Dishevelled is necessary for both interaction with Gbeta2gamma2 and subsequent degradation of Dishevelled via the lysosomal pathway. Signaling induced by Gbeta2gamma2 is required because a mutant of Gbeta2, Gbeta2 (W332A) with lower signaling activity, had reduced ability to downregulate the level of Dishevelled. Activation of Wnt signaling by either of two methods, increased Frizzled signaling or transient transfection of Wnt, also led to increased degradation of Dishevelled and the induced Dishevelled loss is dependent on Gbeta1 and Gbeta2. Other studies with agents that interfere with PLC action and calcium signaling suggested that loss of Dishevelled is mediated through the following pathway: Wnt/Frizzled-->Gbetagamma-->PLC-->Ca+2/PKC signaling. Together the evidence suggests a novel negative feedback mechanism in which Gbeta2gamma2 inhibits Wnt signaling by degradation of Dishevelled.


Assuntos
Proteínas Adaptadoras de Transdução de Sinal/genética , Animais , Blastômeros/citologia , Linhagem Celular , Desenvolvimento Embrionário/genética , Retroalimentação Fisiológica , Receptores Frizzled/genética , Proteínas de Ligação ao GTP/genética , Regulação da Expressão Gênica no Desenvolvimento , Humanos , Mutação , Fosfoproteínas/genética , Ligação Proteica , RNA Interferente Pequeno/genética , Proteínas Repressoras/genética , Transfecção , Proteínas Wnt/genética , Xenopus , Proteínas de Xenopus/genética
7.
Artigo em Inglês | WPRIM (Pacífico Ocidental) | ID: wprim-161891

RESUMO

BACKGROUND/AIMS: This study aimed to better understand gene expression profiles of human hepatic stellate cell (HSC) activation and the relationship with the Wnt signaling pathway. METHODS: The global transcript levels in platelet derived growth factor-BB (PDGF-BB)-stimulated hTERT HSCs were analyzed using oligonucleotide microarrays. Oligonucleotide microarrays with 19K human oligo chips were performed to obtain gene expression profiles associated with proliferation in human hTERT HSCs. The microarray data was verified by real time quantitative PCR and expression of the components of Wnt signaling was analyzed by Western blot. RESULTS: Microarray data showed 243 up-regulated and 265 down-regulated genes in PDGF-BB-treated HSCs. The changes in expression of glypican3 and BH3 interacting domain death agonist (BID) mRNA in real time quantitative PCR, especially among the highly up- or down-regulated genes, were statistically consistent with the microarray data. The Wnt signaling pathway components, frizzled10 (FZD10) and calcium/calmodulin-dependent protein kinase II alpha (CAMK2A), showed increased expression in the short time course microarray and the up-regulation of FZD10 also occurred at the protein level. Our data showed various gene expression profiles during activation of human HSC. CONCLUSIONS: The up-regulated expression of FZD10 and CAMK2A suggests that the Wnt/Ca2+ signaling pathway is active in hTERT HSCs and may participate in HSC activation and proliferation


Assuntos
Indutores da Angiogênese/farmacologia , Western Blotting , Proteína Quinase Tipo 2 Dependente de Cálcio-Calmodulina/genética , Linhagem Celular , Proliferação de Células , Receptores Frizzled/genética , Perfilação da Expressão Gênica , Células Estreladas do Fígado/citologia , Humanos , Análise de Sequência com Séries de Oligonucleotídeos , Fator de Crescimento Derivado de Plaquetas/farmacologia , Reação em Cadeia da Polimerase , Receptores Acoplados a Proteínas-G/genética , Transdução de Sinais , Regulação para Cima , Proteínas Wnt/genética
9.
Braz. oral res ; 21(2): 127-133, 2007. ilus
Artigo em Inglês | LILACS (Américas) | ID: lil-453191

RESUMO

A comparative nonisotopic in situ hybridization (ISH) analysis was carried out for the detection of Bmp-4, Shh and Wnt-5a transcripts during mice odontogenesis from initiation to cap stage. Bmp-4 was expressed early in the epithelium and then in the underlying mesenchyme. Shh expression was seen in the odontogenic epithelial lining thickening, being stronger in the enamel knot area, during the cap stage. Wnt-5a transcripts were expressed only in the mesenchyme during the initiation, bud and cap stages, with strong expression in the dental mesenchyme during the bud stage. The present results showed that Bmp-4, Shh and Wnt-5a are expressed since the very early stages of tooth development, and they suggest that the Wnt-5a gene is expressed in different cell populations than Bmp-4 and Shh.


No presente trabalho, realizou-se uma análise comparativa não isotópica por hibridização in situ a fim de se detectar a presença de transcritos de Bmp-4, Shh e Wnt-5a durante as fases iniciais da odontogênese em camundongos, desde a iniciação até o estágio de capuz. No estágio de iniciação, observou-se expressão precoce de Bmp-4 no epitélio e no mesênquima subjacente, enquanto que a expressão de Shh ocorreu durante o estágio de capuz, na região de espessamento do revestimento epitelial odontogênico, tornando-se mais intensa na área de nó do esmalte. Os transcritos de Wnt-5a foram expressos somente no mesênquima durante os estágios de iniciação, botão e capuz, com intenso sinal na região no mesênquima na fase de botão. Estes resultados mostraram que Bmp-4, Shh e Wnt-5a são expressos desde os estágios mais precoces do desenvolvimento dentário, sugerindo que o gene Wnt-5a seja expresso em populações celulares distintas daquelas que expressam Bmp-4 e Shh.


Assuntos
Animais , Camundongos , Proteínas Morfogenéticas Ósseas/análise , Proteínas Hedgehog/análise , Odontogênese/fisiologia , Proteínas Wnt/análise , Proteínas Morfogenéticas Ósseas/genética , Modelos Animais de Doenças , Regulação da Expressão Gênica no Desenvolvimento , Expressão Gênica/fisiologia , Proteínas Hedgehog/genética , Hibridização In Situ , Odontogênese/genética , Transcrição Genética , Germe de Dente/citologia , Germe de Dente/embriologia , Proteínas Wnt/genética
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