[Corrigendum] Neurotoxin β‑N‑methylamino‑L‑alanine induces endoplasmic reticulum stress‑mediated neuronal apoptosis

Figure 4.

Overexpression of HSP70 suppresses ER stress-mediated neuronal death induced by BMAA, Tg and Tm. Following transfection with DNA constructs of pcDNA and HSP70 for 24 h, the cells were treated with 3.0 mM BMAA, 1 μM Tg, or 10 μg/ml Tm for 24 h. Con cells are untreated cells. (A) Western blotting for ER stress and apoptosis markers was performed. HSP70 was tagged with HA and the expression of HSP70 in the indicated transfectants was analyzed by western blotting. Consistent results are representative of at least three different experiments. (B) Cell viability was measured using an MTT assay. The percentage viability was plotted as the mean ± standard deviation of at least five experiments (*P<0.05 vs. untreated cells; #P<0.05 vs. BMAA-treated cells transfected with pcDNA only). (C) Nuclear morphology was visualized by DAPI nuclear staining. Mock are untransfected cells, and Con are untreated cells. The experiments were performed in triplicate, and cells were visualized under a confocal microscope. (D) The percentage of subG1 cells was analyzed via flow cytometry. The data are expressed as the mean ± standard deviation obtained from at least three independent experiments (*P<0.05 vs. untreated cells; #P<0.05 vs. BMAA-treated cells transfected with pcDNA only). BMAA, β-N-methylamino-L-alanine; Bcl, B-cell lymphoma; Bax, Bcl-2-associated X protein; P-, phosphorylated; ATF, transcription factor 6; ER, endoplasmic reticulum; CHOP, CCAAT/-enhancer-binding protein homologous protein; Tg, thapsigargin; Tm, tunicamycin; HSP, heat shock protein; HA, hemagglutinin; XBP, X-box binding protein; PARP, poly-ADP ribose polymerase; PDI, protein disulfide isomerase; PERK, protein kinase RNA-like endoplasmic reticulum kinase; con, control; eIF2, eukaryotic initiation factor 2.