Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 2 de 2
Filtrar
Mais filtros










Base de dados
Intervalo de ano de publicação
1.
Innate Immun ; 22(8): 682-695, 2016 11.
Artigo em Inglês | MEDLINE | ID: mdl-27688705

RESUMO

Pulmonary alveolar macrophages (AMs) are important in defense against bacterial lung inflammation. Cluster of differentiation 14 (CD14) is involved in recognizing bacterial lipopolysaccharide (LPS) through MyD88-dependent and TRIF pathways of innate immunity. Sulforaphane (SFN) shows anti-inflammatory activity and suppresses DNA methylation. To identify CD14 epigenetic changes by SFN in the LPS-induced TRIF pathway, an AMs model was investigated in vitro. CD14 gene expression was induced by 5 µg/ml LPS at the time point of 12 h and suppressed by 5 µM SFN. After 12 h of LPS stimulation, gene expression was significantly up-regulated, including TRIF, TRAF6, NF-κB, TRAF3, IRF7, TNF-α, IL-1ß, IL-6, and IFN-ß. LPS-induced TRAM, TRIF, RIPK1, TRAF3, TNF-α, IL-1ß and IFN-ß were suppressed by 5 µM SFN. Similarly, DNMT3a expression was increased by LPS but significantly down-regulated by 5 µM SFN. It showed positive correlation of CD14 gene body methylation with in LPS-stimulated AMs, and this methylation status was inhibited by SFN. This study suggests that SFN suppresses CD14 activation in bacterial inflammation through epigenetic regulation of CD14 gene body methylation associated with DNMT3a. The results provide insights into SFN-mediated epigenetic down-regulation of CD14 in LPS-induced TRIF pathway inflammation and may lead to new methods for controlling LPS-induced inflammation in pigs.


Assuntos
Infecções Bacterianas/imunologia , Epigênese Genética/efeitos dos fármacos , Isotiocianatos/farmacologia , Receptores de Lipopolissacarídeos/metabolismo , Macrófagos Alveolares/efeitos dos fármacos , Pneumonia/imunologia , Alvéolos Pulmonares/patologia , Proteínas Adaptadoras de Transporte Vesicular/metabolismo , Animais , Células Cultivadas , Metilação de DNA , Imunidade Inata , Lipopolissacarídeos/imunologia , Macrófagos Alveolares/imunologia , Transdução de Sinais/efeitos dos fármacos , Sulfóxidos , Suínos
2.
BMC Genomics ; 15: 43, 2014 Jan 18.
Artigo em Inglês | MEDLINE | ID: mdl-24438674

RESUMO

BACKGROUND: Low efficiency of Somatic Cell Nuclear Transfer (NT) has been widely addressed with high incidence of placental abnormalities due to genetic and epigenetic modifications. MiRNAs are shown to be major regulators of such modifications. The present study has been carried out to identify the expression patterns of 377 miRNAs, their functional associations and mechanism of regulation in bovine placentas derived from artificial insemination (AI), in vitro production (IVP) and NT pregnancies. RESULTS: This study reveals a massive deregulation of miRNAs as chromosomal cluster or miRNA families without sex-linkage in NT and in-vitro derived IVP placentas. Cell specific localization miRNAs in blastocysts and expression profiling of embryos and placentas at different developmental stages identified that the major deregulation of miRNAs exhibited in placentas at day 50 of pregnancies is found to be less dependent on global DNA methylation, rather than on aberrant miRNA biogenesis molecules. Among them, aberrant AGO2 expression due to hypermethylation of its promoter was evident. Along with other factors, aberrant AGO2 expression was observed to be associated with multiple defects in trophoblast differentiation through deregulation of miRNAs mediated mechanisms. CONCLUSION: These aberrant miRNA activities might be associated with genetic and epigenetic modifications in abnormal placentogenesis due to maldifferentiation of early trophoblast cell lineage in NT and IVP pregnancies. This study provides the first insight into genome wide miRNA expression, their role in regulation of trophoblast differentiation as well as abnormal placental development in Somatic Cell Nuclear Transfer pregnancies to pave the way to improve the efficiency of cloning by nuclear transfer.


Assuntos
Reprogramação Celular , MicroRNAs/metabolismo , Placenta/citologia , Trofoblastos/citologia , Animais , Proteínas Argonautas/antagonistas & inibidores , Proteínas Argonautas/genética , Proteínas Argonautas/metabolismo , Blastocisto/citologia , Blastocisto/metabolismo , Bovinos , Diferenciação Celular , Ilhas de CpG , Metilação de DNA , Embrião de Mamíferos/metabolismo , Feminino , Fertilização in vitro , MicroRNAs/genética , Placenta/metabolismo , Gravidez , Regiões Promotoras Genéticas , Interferência de RNA , RNA Mensageiro/metabolismo , RNA Interferente Pequeno/metabolismo , Células-Tronco/citologia , Células-Tronco/metabolismo , Trofoblastos/metabolismo
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA
...