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. 2011 Jan 5;31(1):247–261. doi: 10.1523/JNEUROSCI.4589-10.2011

Figure 6.

Figure 6.

Critical role of ASK1-JNK/p38 signaling pathway in 6-OHDA neurotoxicity in MN9D cells. A, Knockdown of ASK1 expression in MN9D cells. MN9D cells were infected for 3 d with lentiviral vectors containing shRNA ASK1t or ASK1sc, or GFP cDNA, and then subjected to immunoblotting against ASK1 (top). Cotransfection of ASK1t and the human ASK1 (hASK1) restores the expression level of ASK1 in cells (bottom). B, Knockdown of ASK1 expression in MN9D cells prevents the activation of JNK (p-JNK), c-Jun (p-c-Jun), and p38 (p-p38) at 2 and 8 h after 6-OHDA (50 μm) exposure. C, Quantitative results of (B). *p < 0.05, **p < 0.01 between the groups indicated; data are from four experiments. D–F, Knockdown of ASK1 expression is neuroprotective against 6-OHDA neurotoxicity in MN9D cells (D); cotransfection of hASK1 restores the suppressed (by ASK1t) 6-OHDA neurotoxicity (E); overexpression of ASK1dn promotes cell survival after 6-OHDA neurotoxicity (F). In all experiments described in D–F, cell viability was measured at 24 h after 6-OHDA (50 and 100 μm) exposure. *p < 0.05, **p < 0.01 between the groups indicated; n = 12 from three to four independent experiments.