A rescue factor abolishing neuronal cell death by a wide spectrum of familial Alzheimer's disease genes and Abeta -- Data Supplement - Supplemental Data -- Proceedings of the National Academy of Sciences

Supplementary material for Hashimoto et al. (2001) Proc. Natl. Acad. Sci. USA 98 (11), 6336–6341. (10.1073/pnas.101133498)

Supplemental Figure 8 Fig. 8.
Effect of HN on etoposide-induced cell death in primary cultured neurons. (A) Phase-contrast microscopic views 72 hr after Ab treatment with or without sHN or HN derivatives. Representative views are indicated. Primary cultured cortical neurons were treated with 25 µM Ab 1-43 in the presence or absence of sHN (10 nM, 10 µM), 10 nM sHNG, or 10 µM sHNA. In these experiments, the indicated final concentrations of HN polypeptides were added 16 hr before the onset of treatment with Ab 1-43. Note the formation of Ab aggregates in the panels of experiments in which cells were treated with Ab. The numbers indicated in the bottom right corner are the mortality values of these cells assessed by Trypan blue exclusion assay (means ± SD of three independent experiments). (B) Lack of the effect of HN on neuronal death by low and high concentrations of etoposide. At 72 hr after treatment of primary cultured neurons with various concentrations of etoposide in the presence or absence of 10 µM sHN, cell mortality (Trypan blue exclusion assay; Left) and cell viability (Calcein-AM fluorescence assay in total fluorescence intensity; Right) were measured. Values indicate means ± SD of three independent experiments.