Fig. 3: SCD1 expression decreases during preparation for cell death.

Fibroblasts were cultivated under diverse cytotoxic conditions for 48 h (a–c, e) or as indicated (d). a Cellular proportion of non-esterified SFAs, MUFAs, and PUFAs. SFAs: 12:0, 14:0, 16:0, 18:0; MUFAs: 16:1, 18:1; PUFAs: 18:2, 20:4, 22:5, 22:6 (MUFA LTR P = 0.0146, 0.0128, 0.0023, 0.0155, 0.003; SFA LTR P = 0.0176, 0.0088, 0.0013, 0.0072, 0.0015). b Heatmap showing changes in the free fatty acid profile as compared to vehicle control. Data are given as percentage of the relative free fatty acid abundance. c Volcano plots highlighting free fatty acids that are strongly and significantly modulated by VAL or MC. Comparisons of the indicated treatment groups show the mean difference of percentage changes and the negative log10(adjusted P value). Adjusted P values given vs. vehicle control; two-tailed multiple unpaired student t tests from log data with correction for multiple comparisons using a two-stage linear step-up procedure by Benjamini, Krieger, and Yekutieli (false discovery rate 5%). d Heatmaps showing the time-dependent effect on Scd1, Actb, and Gapdh mRNA levels that were normalized to the total amount of cellular RNA and compared to vehicle control for each time point. e Protein expression of SCD1. Western blots are representative of seven independent experiments (LTR P = 0.000000002, \(0.\bar{99}\)). Mean (b–d) or mean + s.e.m. (a) and single data (e) from n = 2 (d for Scd1 and Gapdh at 6 h; Actb at 48 h for Serum), n = 3 (a–d), n = 6 (e for TNFα, Serum, I3M), n = 7 (e) independent experiments. *P < 0.05, **P < 0.01 or P values given vs. vehicle control; repeated measures one-way ANOVA (a) or mixed-effects model (REML) of log data (e) + Tukey HSD post hoc tests.