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Id: biblio-1041039
Autor: Yao, Yuan; Xiong, Gang; Jiang, Xuejun; Song, Tao.
Título: The overexpression of lncRNA H19 as a diagnostic marker for coronary artery disease
Fonte: Rev. Assoc. Med. Bras. (1992);65(2):110-117, Feb. 2019. graf.
Idioma: en.
Projeto: Natural Science Foundation of Hubei Province.
Resumo: SUMMARY OBJECTIVE: Our study aimed to investigate the diagnostic value of lncRNA H19 for coronary artery disease (CAD) and to explore its possible mechanisms. Methods: A total of 30 CAD patients and 30 healthy individuals, as well as patients with different cardiovascular diseases, were included in this study. Blood was drawn from each participant to prepare serum samples, and the expression of lncRNA H19 was detected using qRT-PCR. The ROC curve analysis was used to analyze the diagnostic value of H19 for CAD. The effects of patients' basic information and lifestyle on H19 expression were analyzed. The plasma level of TGF-β1 was measured by ELISA. The H19 overexpression in the human primary coronary artery endothelial cell (HCAEC) line was constructed, and the effects of H19 overexpression on the TGF-β1 expression were analyzed using Western blot. The results of H19 expression were specifically upregulated in patients with CAD but not in healthy individuals and patients with other types of cardiovascular diseases. The ROC curve analysis showed that the H19 expression level could be used to predict CAD accurately. Gender, age, and patients' lifestyle had no significant effects on H19 expression, but H19 expression was higher in patients with a longer course of disease in comparison with the controls. H19 expression was positively correlated with the serum level of TGF-β1, and H19 overexpression significantly increased TGF-β1 protein level in HCAEC. Conclusion: H19 overexpression participates in the pathogenesis of CAD by increasing the expression level of TGF-β1, and H19 expression level may serve as a diagnostic marker for CAD.

RESUMO OBJETIVO Nosso estudo teve como objetivo investigar o valor diagnóstico do lncRNA H19 para doença arterial coronariana (DAC) e explorar os possíveis mecanismos. Métodos Um total de 30 pacientes com DAC e 30 pessoas saudáveis, bem como pacientes com diferentes doenças cardiovasculares foram incluídos neste estudo. O sangue foi extraído de cada participante para preparar amostras de soro e a expressão de lncRNA H19 foi detectada por qRT-PCR. A análise da curva ROC foi utilizada para analisar o valor diagnóstico de H19 para DAC. Efeitos da informação básica dos pacientes e estilo de vida na expressão de H19 foram analisados. O nível plasmático de TGF-β1 foi medido por ELISA. A linha de células endoteliais da artéria coronária primária (HCAEC) humana de sobre-expressão de H19 foi construída e os efeitos da sobre-expressão de H19 na expressão de TGF-β1 foram analisados por Western blot. Resultados A expressão de H19 foi especificamente regulada positivamente em pacientes com DAC, mas não em pessoas saudáveis e em pacientes com outros tipos de doenças cardiovasculares. A análise da curva ROC mostrou que o nível de expressão de H19 pode ser usado para prever com precisão a DAC. Sexo, idade e estilo de vida dos pacientes não têm efeitos significativos sobre a expressão de H19, mas a expressão de H19 foi maior em pacientes com curso mais longo da doença em comparação com os controles. A expressão de H19 correlacionou-se positivamente com o nível sérico de TGF-β1 e a superexpressão de H19 aumentou significativamente o nível de proteína de TGF-β1 em HCAEC. Conclusão A superexpressão de H19 participa da patogênese da DAC aumentando o nível de expressão de TGF-β1 e o nível de expressão de H19 pode servir como marcador diagnóstico de DAC.
Descritores: Doença da Artéria Coronariana/diagnóstico
Fator de Crescimento Transformador beta1/sangue
RNA Longo não Codificante/sangue
-Doença da Artéria Coronariana/sangue
Ensaio de Imunoadsorção Enzimática
Biomarcadores/sangue
Estudos de Casos e Controles
Regulação para Cima
Curva ROC
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Pessoa de Meia-Idade
Limites: Humanos
Masculino
Feminino
Adulto
Idoso
Responsável: BR1.1 - BIREME


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Id: biblio-1011402
Autor: Wang, Yanqiu; Xiang, Jun; Wang, Jianjun; Ji, Yazhong.
Título: Downregulation of TGF-ß1 suppressed proliferation and increased chemosensitivity of ovarian cancer cells by promoting BRCA1/Smad3 signaling
Fonte: Biol. Res;51:58, 2018. graf.
Idioma: en.
Projeto: National Natural Science Fund of China; . Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases.
Resumo: BACKGROUND: Studies have demonstrated that transforming growth factor beta-1 (TGF-ß1) exhibits oncogenic activity in different types of cancer, including ovarian cancer (OC). However, its regulatory mechanism in OC and whether TGF-ß1 is involved in chemosensitivity regulation remains unclear. Thus, the aim of this study was to investigate the role of TGF-ß1 in OC. METHODS: The OC cell line SKOV3 was employed, and TGF-ß1 overexpression or knockdown vectors were constructed. The cell proliferation of SKOV3 was evaluated with the cell counting kit (CCK8) kit after treatment with different concentrations of cis-platinum. Western blot and protein immunoprecipitation were employed to detect changes in BRCA1 and Smad3 expression and their interactions. Tumor growth in nude mice was evaluated. RESULTS: The results showed that TGF-ß1 knockdown increased chemosensitivity by promoting BRCA1 expression and Smad3 phosphorylation. In vivo studies showed that TGF-ß1 knockdown significantly inhibited the growth of tumors, also by upregulating BRCA1 expression and Smad3 phosphorylation. CONCLUSION: Taken together, our results suggest that TGF-ß1 knockdown inhibits tumor growth and increases chemosensitivity by promotion of BRCA1/Smad3 signaling.
Descritores: Neoplasias Ovarianas/metabolismo
Regulação para Baixo/fisiologia
Genes BRCA1/fisiologia
Proteína Smad3/fisiologia
Fator de Crescimento Transformador beta1/fisiologia
-Neoplasias Ovarianas/patologia
Neoplasias Ovarianas/tratamento farmacológico
Imuno-Histoquímica
Células Cultivadas
Western Blotting
Resistencia a Medicamentos Antineoplásicos/fisiologia
Proteínas Supressoras de Tumor/fisiologia
Linhagem Celular Tumoral
Proliferação de Células
Proteína Smad3/análise
Fator de Crescimento Transformador beta1/análise
Técnicas de Silenciamento de Genes
Reação em Cadeia da Polimerase em Tempo Real
Camundongos Endogâmicos BALB C
Limites: Humanos
Animais
Masculino
Feminino
Responsável: CL1.1 - Biblioteca Central


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Cardoso, Maria Regina Alves
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Id: lil-583370
Autor: Coelho, Verônica Porto Carreiro de Vasconcellos; Ioschpe, Rafael; Caldas, Cristina; Spadafora-Ferreira, Monica; Fonseca, João Americo; Cardoso, Maria Regina Alves; Palacios, Selma Aliotti; Kalil, Jorge; Goldberg, Anna Carla.
Título: Contrasting roles of donor and recipient TGFB1 and IFNG gene polymorphic variants in chronic kidney transplant rejection / Papéis contrastantes das variantes polimórficas dos genes TGFB1 e IFNG do doador e do receptor na rejeição crônica de transplantados renais
Fonte: Einstein (Säo Paulo);9(1), jan.-mar. 2011. tab.
Idioma: en; pt.
Resumo: Objective: To assess the long-term impact (minimum of 3 years follow-up) of polymorphisms in cytokine genes in donor: recipient pairs on the results of the transplant. Methods: We compared genetic cytokine polymorphisms and the primary factors of risk for the development of chronic rejection in paired groups of renal transplant patients with and without chronic allograft nephropathy [CAN]. Results: Multivariate analysis indicated that the presence of the high-production TT genotype (codon 10) of the transforming growth factor beta-1 (TGFB1) was protective in receptors (p=0.017), contrasting with the increased risk when present in donor samples (p=0.049). On the other hand, in the case of the gamma interferon studied, the greater frequency of the high production allele was protective in the analysis of the donor group (p=0.013), increasing the risk of chronic nephropathy of the allograft when present in the recipients (p=0.036). Conclusion: Our results highlight the importance of TGFB1 genotyping in donors, and indicate that polymorphisms in the gene of this cytokine in donor cells might contribute to the development of chronic allograft nephropathy.

Objetivo: Avaliar o impacto de longo prazo (com seguimento mínimo de 2 anos) de polimorfismos em genes de citocinas em pares doador:receptor sobre os resultados do transplante. Métodos: Comparamos os polimorfismos genéticos das citocinas e os principais fatores de risco para o desenvolvimento de rejeição crônica em grupos pareados de pacientes transplantados renais com e sem nefropatia crônica do aloenxerto [CAN]. Resultados: A análise multivariada indicou que a presença do genótipo TT (códon 10) de alta produção do fator de crescimento transformador beta-1 (TGFB1) era protetor nos receptores (p=0,017), em contraste com o risco aumentado quando presente nas amostras de doadores (p=0,049). Por outro lado, no caso do interferon gama estudado, a maior frequência do alelo de alta produção foi protetora na análise do grupo de doadores (p=0,013), mas aumentava o risco de nefropatia crônica do aloenxerto quando presente nos receptores (p=0,036). Conclusão: Nossos resultados ressaltam a importância da genotipagem de TGFB1 também em doadores, e indicam que polimorfismos no gene desta citocina em células do doador podem contribuir no desenvolvimento da nefropatia crônica do aloenxerto.
Descritores: Fator de Crescimento Transformador beta1
Genótipo
Interferon gama
Polimorfismo Genético
Transplante Homólogo
Tipo de Publ: Estudo Comparativo
Responsável: BR500.1 - Biblioteca


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Id: lil-798103
Autor: Shaker, Olfat G; Alnoury, Amina M; Hegazy, Gehan A; El Haddad, Hemmat E; Sayed, Safaa; Hamdy, Ahmed.
Título: Methylene tetrahydrofolate reductase, transforming growth factor-ß1 and lymphotoxin-α genes polymorphisms and susceptibility to rheumatoid arthritis / Polimorfismos dos genes metilenotetrahidrofolato redutase, fator de crescimento transformador β1 e linfotoxina-α e susceptibilidade à artrite reumatoide
Fonte: Rev. bras. reumatol;56(5):414-420, Sept.-Oct. 2016. tab, graf.
Idioma: en.
Resumo: ABSTRACT Background: Rheumatoid arthritis is a widely prevalent autoimmune disorder with suggested genetic predisposition. Objectives: The aim of this study is to detect the pattern of genetic polymorphism of methylene tetrahydrofolate reductase (MTHFR C677 T and A1298 C), transforming growth factor-β1 (TGF-β1 T869 C) and lymphotoxin-α (LT-α A252G) in patients having rheumatoid arthritis and correlate these patterns to disease activity and serum levels of tumor necrosis factor-alpha (TNF-α), B-Cell Activating Factor (BAFF), and osteopontin. Methods: A total of 194 subjects, 90 controls and 104 patients with rheumatoid arthritis were genotyped for MTHFR C677 T and A1298 C, TGF-β1 T869 C and LT-α A252G polymorphisms using a methodology based on PCR-RFLP. Also serum levels of TNF-α, osteopontin and BAFF were measured by ELISA kits. Results: The CT genotype and T allele of MTHFR C677 T and GG genotype and G allele of LT-α A252G are associated with the risk of RA and with higher levels of the pro-inflammatory cytokine, TNF-α in patients with rheumatoid arthritis. Conclusion: Our findings suggest that there is association between MTHFR C677 T and LT-α A252G genes polymorphisms and increased risk of RA in this sample of Egyptian population.

RESUMO Antecedentes: A artrite reumatoide é uma doença autoimune amplamente prevalente com sugerida predisposição genética. Objetivos: Detectar o padrão de polimorfismo dos genes metilenotetrahidrofolato redutase (MTHFR C677 T e A1298 C), fator de crescimento transformador β1 (TGF-β1 T869 C) e linfotoxina-α (LT-α A252G) em pacientes com artrite reumatoide e correlacionar esses padrões com a atividade da doença e os níveis séricos de fator de necrose tumoral alfa (TNF-α), fator ativador de linfócitos B (BAFF) e osteopontina. Métodos: Foram genotipados 194 indivíduos – 90 controles e 104 com artrite reumatoide – à procura de polimorfismos dos genes MTHFR C677 T e A1298 C, TGF-β1 T869 C e LT-α A252G com uma metodologia baseada na PCR-RFLP. Mensuraram-se também os níveis séricos de TNF-α, osteopontina e BAFF com kits de Elisa. Resultados: O genótipo CT e o alelo T do MTHFR C677 T e o genótipo GG e alelo G do LT-α A252G estão associados ao risco de AR e a níveis mais elevados da citocina pró-inflamatória TNF-α em pacientes com artrite reumatoide. Conclusão Os achados do presente estudo sugerem que há associação entre os polimorfismos dos genes MTHFR C677 T e LT-α A252G e um risco aumentado de AR nessa amostra da população egípcia.
Descritores: Artrite Reumatoide/genética
Linfotoxina-alfa/genética
Metilenotetra-Hidrofolato Redutase (NADPH2)/genética
Fator de Crescimento Transformador beta1/genética
-Artrite Reumatoide/epidemiologia
Fatores de Crescimento Transformadores
Predisposição Genética para Doença/genética
Polimorfismo de Nucleotídeo Único/genética
Egito
Limites: Humanos
Responsável: BR1.1 - BIREME


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Amantea, Sergio Luis
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Id: biblio-886258
Autor: Silva, Samanta Sarmento da; Peterson, Guilherme Eckert; Amantéa, Sérgio Luis; Miorelli, Patrícia; Ulbrich, Jane Maria; Roesch, Eliane; Sanches, Paulo Roberto; Fraga, Jose Carlos.
Título: Transforming growth factor beta1 (TGF-ß1) levels in a rat model of induced pleural empyema
Fonte: Acta cir. bras;33(2):156-162, Feb. 2018. tab, graf.
Idioma: en.
Resumo: Abstract Purpose: To evaluate the concentration of transforming growth factor beta 1 (TGFB1) levels in a rat pleural effusion obtained by inoculation of intrapleural bacteria or turpentine through thoracentesis. Methods: Thirty-Nine Wistar rats were divided into three groups: Staphylococcus aureus (SA, n = 17); Streptococcus pneumoniae (SP, n = 12); and turpentine (control, n = 10). Pleural fluid was collected through ultrasound-guided thoracentesis 12 h, 24 h, and 36 h after instillation of bacteria or turpentine. Levels of TGFB1 were measured in pleural fluid. Results: At 12 h, mean TGFB1concentrations were 5.3450 pg/mL in the SA group, 5.3449 pg/mL in the SP group, and 5.3450 pg/mL in controls. At 24 h, they were 4.6700 pg/mL in the SA group, 4.6700 pg/mL in the SP group, and 4.6700 pg/mL in controls. At 36 h, they were 4.6699 pg/mL in the SA group and in control. No difference was observed among the groups in mean TGFB1concentration (p = 0.12); however, a significant intragroup reduction in mean TGFB1 was observed between 12 and 24 h (p < 0.01). Conclusion: The transforming growth factor beta 1 concentrations were not useful as a diagnostic tool or an early marker of infected pleural effusion.
Descritores: Derrame Pleural/diagnóstico
Empiema Pleural/diagnóstico
Fator de Crescimento Transformador beta1/análise
-Derrame Pleural/complicações
Bactérias/patogenicidade
Biomarcadores/análise
Empiema Pleural/complicações
Empiema Pleural/microbiologia
Ratos Wistar
Modelos Animais de Doenças
Limites: Animais
Masculino
Ratos
Responsável: BR1.1 - BIREME


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Id: biblio-886197
Autor: Zhang, Chong; Liu, Yu-Jie.
Título: Biomechanic and histologic analysis of fibroblastic effects of tendon to bone healing by transforming growth factor ß1 (TGF-ß1) in rotator cuff tears
Fonte: Acta cir. bras;32(12):1045-1055, Dec. 2017. graf.
Idioma: en.
Projeto: Hebei Province Science and Technology Project.
Resumo: Abstract Purpose: To evaluate the effect of transforming growth factor β1 (TGF-β1) on tendon-to-bone reconstruction of rotator cuff tears. Methods: Seventy-two rat supraspinatus tendons were transected and reconstructed in situ. At 8 and 16 weeks, specimens of three groups; that is control, L-dose (low dose), and H-dose (high dose) were harvested and underwent a biomechanical test to evaluate the maximum load and stiffness values. Histology sections of the tendon-to-bone interface were identified by hematoxylin-eosin or Masson trichrome stain. Collagen type III was observed by picric acid sirius red staining under polarized light. The level of insulin-like growth factor 1 (IGF-1) and vascular endothelial growth factor (VEGF) was measured by the enzyme-linked immunosorbent assay (ELISA) method. Results: Collagen type III of the H-dose group had a significant difference in histology structure compared with the L-dose group (P<0.05). The maximum load and stiffness decreased significantly in the control group compared with the values of the L-dose and H-dose groups. The stiffness among the three groups differed significantly at the same postoperative time (P<0.05). Interestingly, progressive reestablishment of collagen type III affected tendon-to-bone healing significantly in the later stages. Conclusion: The H-dose was associated with an increased collagen type III morphology stimulated by TGF-β1.
Descritores: Traumatismos dos Tendões/tratamento farmacológico
Cicatrização/fisiologia
Manguito Rotador/cirurgia
Fatores de Crescimento do Endotélio Vascular/metabolismo
Fator de Crescimento Transformador beta1/metabolismo
Lesões do Manguito Rotador/cirurgia
-Traumatismos dos Tendões/metabolismo
Resistência à Tração/fisiologia
Cicatrização/efeitos dos fármacos
Fenômenos Biomecânicos
Ensaio de Imunoadsorção Enzimática
Manguito Rotador/metabolismo
Ratos Sprague-Dawley
Colágeno Tipo III/metabolismo
Modelos Animais de Doenças
Elasticidade/fisiologia
Fator de Crescimento Transformador beta1/farmacologia
Força Muscular/fisiologia
Fibroblastos/efeitos dos fármacos
Fibroblastos/fisiologia
Lesões do Manguito Rotador/metabolismo
Limites: Animais
Masculino
Ratos
Responsável: BR1.1 - BIREME


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Id: biblio-886274
Autor: Wu, Jing; Pan, Lin; Jin, Xueqin; Li, Weihua; Li, Hongbing; Chen, Jianmao; Yang, Wen.
Título: The role of oxymatrine in regulating TGF-ß1 in rats with hepatic fibrosis
Fonte: Acta cir. bras;33(3):207-215, Mar. 2018. tab, graf.
Idioma: en.
Projeto: Ningxia Natural Science Foundation; . School Level Project of Ningxia Medical University.
Resumo: Abstract Purpose: To investigate whether oxymatrine (OMT) prevents hepatic fibrosis in rats by regulating liver transforming growth factor β1 (TGF-β1) level. Methods: Hepatic fibrosis was induced in rats by thioacetamide (TAA). Blood was collected at the end of week 12 to determine the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and glutathione (GSH). Changes in liver tissue were observed after hematoxylin-eosin (HE) staining. Results: Fibrosis was confirmed by Masson's collagen staining. Liver TGF-β1 level was determined by ELISA. OMT significantly reduced serum ALT and AST but increased GSH levels in rats with hepatic fibrosis. Moreover, it significantly improved liver histology in rats with TAA-induced hepatic fibrosis. It significantly decreased liver TGF-β1 level compared to that in the untreated group. It also significantly reduced collagen deposition in rats. Conclusion: Oxymatrine is effective in protecting rats from thioacetamide-induced hepatic fibrosis by regulating TGF-β1 expression.
Descritores: Quinolizinas/farmacologia
Substâncias Protetoras/farmacologia
Alcaloides/farmacologia
Fator de Crescimento Transformador beta1/metabolismo
Cirrose Hepática Experimental/prevenção & controle
-Aspartato Aminotransferases/sangue
Ratos Sprague-Dawley
Fator de Crescimento Transformador beta1/efeitos dos fármacos
Cirrose Hepática Experimental/induzido quimicamente
Cirrose Hepática Experimental/metabolismo
Limites: Animais
Masculino
Ratos
Responsável: BR1.1 - BIREME


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Id: biblio-989051
Autor: Zhang, Guangming; Cui, Guanghua; Tong, Shuangxi; Cao, Qingxian.
Título: Salvianolic acid A alleviates the renal damage in rats with chronic renal failure
Fonte: Acta cir. bras;34(2):e201900204, 2019. tab, graf.
Idioma: en.
Resumo: Abstract Purpose: To investigate the protective effects of salvianolic acid A (SAA) on renal damage in rats with chronic renal failure (CRF). Methods: The five-sixth nephrectomy model of CRF was successfully established in group CRF (10 rats) and group CRF+SAA (10 rats). Ten rats were selected as sham-operated group (group S), in which only the capsules of both kidneys were removed. The rats in group CRF+SAA were intragastrically administrated with 10 mg/kg SAA for 8 weeks. The blood urine nitrogen (BUN), urine creatinine (Ucr), creatinine clearance rate (Ccr), and serum uperoxide dismutase (SOD) and malondialdehyde (MDA) were tested. The expressions of transforming growth factor-β1 (TGF-β1), bone morphogenetic protein 7 (BMP-7) and Smad6 protein in renal tissue were determined. Results: After treatment, compared with group CRF, in group CRF+SAA the BUN, Scr, serum MDA and kidney/body weight ratio were decreased, the Ccr and serum SOD were increased, the TGF-β1 protein expression level in renal tissue was decreased, and the BMP-7 and Smad6 protein levels were increased (all P < 0.05). Conclusion: SAA can alleviate the renal damage in CRF rats through anti-oxidant stress, down-regulation of TGF-β1 signaling pathway and up-regulation of BMP-7/Smad6 signaling pathway.
Descritores: Ácidos Cafeicos/uso terapêutico
Proteína Smad6/metabolismo
Fator de Crescimento Transformador beta1/metabolismo
Proteína Morfogenética Óssea 7/metabolismo
Falência Renal Crônica/tratamento farmacológico
Lactatos/uso terapêutico
-Regulação para Baixo
Regulação para Cima
Ratos Sprague-Dawley
Modelos Animais de Doenças
Falência Renal Crônica/induzido quimicamente
Falência Renal Crônica/metabolismo
Testes de Função Renal
Nefrectomia
Limites: Animais
Masculino
Ratos
Responsável: BR1.1 - BIREME


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Id: biblio-837986
Autor: Gaspar, Neide Kalil.
Título: DHEA and frontal fibrosing alopecia: molecular and physiopathological mechanisms
Fonte: An. bras. dermatol;91(6):776-780, Nov.-Dec. 2016.
Idioma: en.
Resumo: Abstract The transforming growth factor-beta 1 (TGFβ1) promotes fibrosis, differentiating epithelial cells and quiescent fibroblasts into myofibroblasts and increasing expression of extracellular matrix. Recent investigations have shown that PPAR (peroxisome proliferator-activated receptor*) is a negative regulator of fibrotic events induced by TGFβ1. Dehydroepiandrosterone (DHEA) is an immunomodulatory hormone essential for PPAR functions, and is reduced in some processes characterized by fibrosis. Although scarring alopecia characteristically develops in the female biological period in which occurs decreased production of DHEA, there are no data in the literature relating its reduction to fibrogenic process of this condition. This article aims to review the fibrogenic activity of TGFβ1, its control by PPAR and its relation with DHEA in the frontal fibrosing alopecia.
Descritores: Desidroepiandrosterona/fisiologia
Alopecia/fisiopatologia
Alopecia/patologia
-Fibrose
PPAR gama/fisiologia
Alopecia/etiologia
Alopecia/terapia
Fator de Crescimento Transformador beta1/fisiologia
Fibroblastos/fisiologia
Fibroblastos/patologia
Líquen Plano/patologia
Limites: Humanos
Feminino
Tipo de Publ: Revisão
Responsável: BR1.1 - BIREME


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Id: biblio-840044
Autor: Shuiai, Zhao; Huijun, Shen; Weizhong, Gu; Aimin, Liu; Jianhua, Mao.
Título: Evaluation of TGF-beta1 and MCP-1 expression and tubulointerstitial fibrosis in children with Henoch-Schönlein purpura nephritis and IgA nephropathy: A clinical correlation
Fonte: Clinics;72(2):95-102, Feb. 2017. tab, graf.
Idioma: en.
Projeto: National Natural Foundation; . Specialized Research Fund for the Doctoral Program of Higher Education; . Natural Science Foundation of Zhejiang Province; . Medicine & Health Technology Innovation Project of Zhejiang Province.
Resumo: OBJECTIVES: Henoch-Schönlein purpura nephritis and immunoglobulin A nephropathy are two diseases with similar clinical presentations but very different prognoses. Transforming growth factor β1 and monocyte chemoattractant protein-1 have been associated with the development of tissue fibrosis. We examined the development of tubulointerstitial fibrosis and its relationship with Transforming growth factor β1 and monocyte chemoattractant protein-1 expression in these patients. METHODS: Renal tissue samples were collected by renal biopsy from 50 children with Henoch-Schönlein purpura nephritis and 50 children with immunoglobulin A nephropathy. Hematoxylin and eosin and Masson's trichrome-stained tissues were examined using light microscopy. Tubulointerstitial fibrosis was graded using the method described by Bohle et al. (1). The immunohistochemical detection of Transforming growth factor β1 and monocyte chemoattractant protein-1 expression was correlated with the tubulointerstitial fibrosis grade. Clinical Trial registration number: ZJCH-2012-0105. RESULTS: Transforming growth factor β1 and monocyte chemoattractant protein-1 expression in the renal tissues was significantly greater in the patients with immunoglobulin A nephropathy than in the patients with Henoch-Schönlein purpura nephritis (both p<0.001). The immunoglobulin A nephropathy patients had a higher tubulointerstitial fibrosis grade than the Henoch-Schönlein purpura nephritis patients (p<0.001). The tubulointerstitial fibrosis grade was in accordance with the Transforming growth factor β1 and monocyte chemoattractant protein-1 expression levels in both diseases (both p<0.001). CONCLUSION: Transforming growth factor β1 and monocyte chemoattractant protein-1 expression was associated with the development of immunoglobulin A nephropathy and Henoch-Schönlein purpura nephritis. Further studies are needed to better evaluate this association.
Descritores: Púrpura de Schoenlein-Henoch/metabolismo
Quimiocina CCL2/metabolismo
Fator de Crescimento Transformador beta1/metabolismo
Glomerulonefrite por IGA/metabolismo
Túbulos Renais/metabolismo
-Prognóstico
Púrpura de Schoenlein-Henoch/patologia
Fibrose
Glomerulonefrite por IGA/patologia
Túbulos Renais/patologia
Limites: Humanos
Masculino
Feminino
Pré-Escolar
Criança
Adolescente
Tipo de Publ: Estudo de Avaliação
Responsável: BR1.1 - BIREME



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BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde