Increased postischemic brain injury in mice deficient in uracil-DNA glycosylase
J. Clin. Invest. Matthias Endres, et al. 113:1711 doi:10.1172/JCI20926 [Go to this article.]

Figure 3
Increased cell death in Ung^–/– neurons after oxygen-glucose deprivation. Primary cortical neurons were prepared from E17 mouse embryos. After 10 days in vitro, cells were exposed to OGD for 120 minutes. (A) LDH release into the culture medium was measured as a marker of cell death at different time points after OGD. Similar results were obtained with phase-contrast microscopy (not shown). (B) Reduction in MTT metabolism was measured 1, 3, 9, and 24 hours after OGD. (C) and (E) TMRE fluorescence measurements revealed an early and enhanced loss of mitochondrial potential (Ø_ψm) present 1 hour after reoxygenation only in Ung^–/– neurons. (D) and (F) Fluorescein diacetate (FD) (green) and propidium-iodide staining (PI) (red) were used to count viable and dead cells after 24 hours. In control cultures, there were no significant differences between Ung^+/+ and Ung^–/– neurons for basal LDH-release, MTT-metabolism, or TMRE-fluorescence. Data are mean ± SEM of two to three independent experiments. *P < 0.001, ^#P < 0.05; ANOVA plus Tukey post hoc test. Scale bar: 50 ∝m.