Fig. 1: Mithramycin’s neuroprotective effects are cell death model-specific.
From: Mithramycin selectively attenuates DNA-damage-induced neuronal cell death
a RCN were treated with varying doses of mithramycin (Mith) +/−50 µM etoposide (Etop). LDH release and calcein signal were measured after 24 h of treatment. b RCN were treated with 50 µM etoposide and/or 200nM mithramycin. Treatment media was replaced with conditioned media at 24h. LDH release and calcein signal were measured 24, 48, and 72 h after treatment. c–f RCN were treated with 200 nM doxorubicin (Dox) (c), 10µM camptothecin (Campto) (d), 0.5 µM staurosporine (Stauro) (e), or 50 µM C2-ceramide (C2-Cer) (f) with or without varying doses of mithramycin. n = 5+/group for all groups. Data represent mean± SD. Significance assigned based on one-way ANOVA and Tukey post hoc test or Brown–Forsythe ANOVA and Dunnett’s T3 multiple comparisons test [a LDH, b LDH Day 1, calcein Day 3, c, d, f Calcein]; *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001 vs control; ^p < 0.05, ^^p < 0.01, ^^^p < 0.001, ^^^^p 0.0001 vs etoposide alone.
