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. Author manuscript; available in PMC: 2014 Jan 1.
Published in final edited form as: J Biochem Mol Toxicol. 2012 Nov 6;27(1):28–41. doi: 10.1002/jbt.21440

Figure 2. UVC exposure increases LC3II formation without changes in mitochondrial mass.

Figure 2

LC3II protein was quantified by Western blot in control and UVC treated cells with and without bafilomycin and normalized to beta-actin. (a) Steady-state (no bafilomycin) levels of LC3II were significantly decreased by UVC exposure at 24, 48 and 72 h when compared to time point controls (asterisks; two-way ANOVA, effect of treatment P = 0.0325). With bafilomycin, UVC exposed cells accumulated more LC3II compared to bafilomycin treated controls at all time points (hash; two-way ANOVA, effect of treatment P = 0.007). (b) MAPLC3 mRNA expression increased by 1.3 fold with UVC exposure 48 h after exposure (asterisks; two-way ANOVA, treatment × time point P = 0.03; Fisher’s PLSD, effect of treatment P < 0.0424 at 48 h). The black line signifies baseline expression level. (c) Representative immunoblots of LC3II in control and UVC (10 J/m2) exposed cells with and without bafilomycin at 24, 48 and 72 h. (d) No significant change in mitochondrial mass was detected after UVC exposure compared to controls (two-way ANOVA, effect of recovery P < 0.0001, treatment × recovery P = 0.4730). (e) mRNA expression of PGC1a, NRF1 and TFAM, COXIV and COXI. NRF1 expression decreased at 6 h (P = 0.0466). TFAM expression was induced 1.3 fold at 6 h but reduced by -1.20 fold by 48 h (two-way ANOVA, treatment × time point P = 0.01; Fisher’s PLSD, effect of treatment P < 0.05 at 6 and 48 h). Bars ± s.e.m.