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Figure 3 | Molecular Neurodegeneration

Figure 3

From: Beta-amyloid increases the expression level of ATBF1 responsible for death in cultured cortical neurons

Figure 3

ATBF1 knockdown decreases the viability of primary cortical neurons upon treatment with Aβ1-42, etoposide (Etop), or homocysteine (Hom). A and C, knockdown of ATBF1 in primary cortical neurons. Primary cortical neurons were transfected with ATBF1 siRNA-1 or control siRNA for 48 h. After transfection, the cells were then incubated in the presence or absence of 10 μM Aβ1-42 (A), 1 μM etoposide (C), or 250 μM homocysteine (C) for 16 h. The expression levels of ATBF1 and actin were determined by Western blot analysis using the anti-ATBF1 and anti-actin antibodies. B and D, primary cortical neurons were seeded at a density of 1 × 106 cells/ml in poly-d-lysine-coated 96-well plates. Three days after plating, cells were transfected with ATBF1 siRNA-1 or control siRNA for 48 h, and the cells were then treated with 0, 2.5, 5, or 10 μM Aβ1-42 (B), 1 μM etoposide (D), or 250 μM homocysteine (D) for 16 h. Cell viability was determined using a CellTiter-Glo luminescent cell viability assay kit and is shown as a percentage of surviving cells. All the values are presented as the mean ± SEM of three independent experiments. *p < 0.05, **p < 0.01 vs control siRNA treatment. N.S., not significant, as determined by Student's t-test.

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