Figure 8

Mitochondrial Ca2+ and cell death are regulated by mitoKCa channel opening in HT1080/BI-1.
(A) HT1080/Neo and HT1080/BI-1 cells were loaded with Rhod II AM and then treated with 5 μM thapsigargin in the presence or absence of NS1619. Rhod II was subsequently monitored. (B) Quantification of Rhod II fluorescence peaks. *, p < 0.05 versus thapsigargin-treated HT1080/Neo. HT1080/Neo and HT1080/BI-1 were treated with 5 μM thapsigargin (C) or 5 μg/ml tunicamycin (D) in the presence or absence of 100 μM diazoxide, 500 μM 5-HD, 100 μM NS1619, or 2 μM paxilline for 48 hrs. Cell viability was measured by trypan blue exclusion. *, p < 0.05 versus thapsigargin-treated HT1080/Neo;#, p < 0.05 versus thapsigargin-treated HT1080/BI-1. $, p < 0.05 versus tunicamycin-treated HT1080/Neo; &, p < 0.05 versus tunicamycin-treated HT1080/BI-1. 5-HD, 5-hydroxydecanoate; DZ, diazoxide; NS, NS1619; 5HD, 5-hydroxydecanoate; Neo, neomycin-resistant pcDNA3-transfected HT1080 cells (HT1080/Neo); BI-1, HA-BI-1-pcDNA3-transfected HT1080 cells (HT1080/BI-1).