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. 2005 Feb 2;25(5):1149–1158. doi: 10.1523/JNEUROSCI.4736-04.2005

Figure 3.

Figure 3.

Suppression of endogenous Bcl-w expression exacerbates Aβ-induced neuronal death. Primary neuron cultures were transfected for 1 or 3 d with siRNA that either specifically targeted Bcl-w [siBcl-w(73), siBcl-w(362)] or served as scrambled or mismatched controls. A, The specific Bcl-w siRNAs but not the control siRNAs decreased endogenous Bcl-w mRNA expression as detected by RT-PCR using rat-specific primers (top). β-Actin served as internal control (bottom). B, Protein levels of Bcl-w were similarly affected by the siRNA treatments, as determined by Western blot with Bcl-w antibody (top).β-Tubulin served as a control (bottom). The picture shown is a representative of duplicated experiments. C, Relative amounts of Bcl-w were determined by densitometric scanning of Western blots from three independent experiments. Data is represented as a mean ± SEM percentage of ncBcl-w (1 d) control values. Significance is defined as **p < 0.01 relative to respective ncBcl-w control group. D, Neuron cultures were exposed for 48 h to 25 μm Aβ25-35 24 h after transfection with siRNA. Data show mean ± SEM cell viability from a representative experiment (n = 6). Significance is defined as **p < 0.01 in comparison to ncBcl-w condition.