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Effects of hypoxia inducible factors-1alpha on autophagy and invasion of trophoblasts / 대한생식의학회지
Article en En | WPRIM | ID: wpr-30941
Biblioteca responsable: WPRO
ABSTRACT
OBJECTIVE: This study was undertaken to determine the effect of hypoxia inducible factor (HIF)-1alpha on the cell death, autophagy, and invasion of trophoblasts. METHODS: To understand the effect of HIF-1alpha, we inhibited HIF-1alpha using siRNA under normoxia and hypoxia conditions. Invasion assay and zymography were performed to determine changes in the invasion ability of HIF-1alpha. Western blotting and immunofluorescence were performed to determine some of the signal events involved in apoptosis and autophagy. RESULTS: There was no difference in cell death through the inhibition of HIF-1alpha expression by siRNA; however, the expression of LC3 and autophagosome formation increased. On the other hand, autophagy was increased, and the invasive ability of trophoblast cells decreased according to the inhibition of HIF-1alpha expression by siRNA. These experimental results mean that HIF-1alpha genes regulate the invasive ability of trophoblasts by increasing autophagy. CONCLUSION: This study contributes important data for understanding the mechanism of early pregnancy implantation and the invasive ability of trophoblasts by defining the relationship between the roles of HIF-1alpha and autophagy.
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Texto completo: 1 Índice: WPRIM Asunto principal: Placenta / Autofagia / Trofoblastos / Western Blotting / Técnica del Anticuerpo Fluorescente / Muerte Celular / Apoptosis / ARN Interferente Pequeño / Mano / Hipoxia Límite: Pregnancy Idioma: En Revista: Clinical and Experimental Reproductive Medicine Año: 2012 Tipo del documento: Article
Texto completo: 1 Índice: WPRIM Asunto principal: Placenta / Autofagia / Trofoblastos / Western Blotting / Técnica del Anticuerpo Fluorescente / Muerte Celular / Apoptosis / ARN Interferente Pequeño / Mano / Hipoxia Límite: Pregnancy Idioma: En Revista: Clinical and Experimental Reproductive Medicine Año: 2012 Tipo del documento: Article