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IFN-gamma Regulates Expression of BRG1 Associated Factor 155/170 and Sensitivity to Steroid in Astrocytes
Immune Network ; : 224-228, 2004.
Artículo en Inglés | WPRIM | ID: wpr-13654
ABSTRACT

BACKGROUND:

The expression of BRG1 associated factors (BAF) 155 and BAF 170 in response to IFN-gamma or TNF-alpha was studied in astrocytoma cell lines and primary astrocytes. BAFs are complexed with BRG1 and are also associated with activated glucocorticoid for glucocorticoid trans-activation.

METHODS:

IFN-gamma was pretreated for 18 hrs and cells were incubated with IL-1 or TNF-alpha for 72 hrs or 96 hrs with different concentrations of steroid. Cell death was measured by LDH assay. BAF expression was assayed by RT-PCR.

RESULTS:

IFN-gamma increased cell death by dexamethasone in LN215 cells but not in LN319 cells. The IFN-gamma increased the expression of BAF 155 and BAF 170 in adult astrocytes and LN215 cells, but IFN-gamma decreased the expression of BAF 155/170 in LN319 cells. The effect of IFN-gamma on the expression of BAF was not as clear in fetal astrocytes as it was in adult astrocytes.

CONCLUSION:

Our results suggest cytokines produced during immune reaction or immunotherapy may modulate steroid susceptibility of astrocytes and astrocytoma cells by influencing the expression of BAFs.
Asunto(s)

Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Astrocitoma / Dexametasona / Línea Celular / Astrocitos / Citocinas / Interleucina-1 / Factor de Necrosis Tumoral alfa / Muerte Celular / Inmunoterapia Tipo de estudio: Estudio diagnóstico Límite: Adulto / Humanos Idioma: Inglés Revista: Immune Network Año: 2004 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Astrocitoma / Dexametasona / Línea Celular / Astrocitos / Citocinas / Interleucina-1 / Factor de Necrosis Tumoral alfa / Muerte Celular / Inmunoterapia Tipo de estudio: Estudio diagnóstico Límite: Adulto / Humanos Idioma: Inglés Revista: Immune Network Año: 2004 Tipo del documento: Artículo