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. 2013 Oct 10;2(11):819–829. doi: 10.5966/sctm.2013-0069

Figure 6.

Figure 6.

Glycosylphosphatidylinositol-anchored protein (GPI-AP)-deficient blood cells derived from FPHR-KP cells are resistant to proaerolysin. (A): Blood cells derived from parental hFib2-iPS5 or FPHR-KP embryoid bodies (EBs) following withdrawal of doxycycline (GPI-AP−) were exposed to 1 nM AE for up to 50 minutes, and viable cells were counted in triplicate using an inverted microscope. After AE treatment, cell viability in hFib2-iPS5 cells (▴) was significantly decreased with time compared with FPHR-KP (○) cells. (B): Following AE treatment, the cells were treated with annexin V-fluorescein isothiocyanate/phosphatidylinositol and analyzed by flow cytometry, which revealed CD59+ cells from hFib2-iPS5 undergoing apoptosis (top right) and CD59− cells of FPHR-KP, which were resistant to apoptosis (bottom right). (C): Representative CFU colonies derived from hFib2-iPS5 and FPHR-KP cells. The cells derived from hFib2-iPS5 EBs and FPHR-KP EBs were cultured in MethoCult methylcellulose medium (StemCell Technologies) with or without proaerolysin. After 14 days, CFUs were counted, and there were no proaerolysin-resistant CFUs in hFib2-iPS5 cells. However, proaerolysin-resistant CFU colonies were observed from FPHR-KP cells. Furthermore, there was no significant difference with or without AE in FPHR-KP cell-derived CFU colonies (p > .05). *, p < .05; **, p < .01. Abbreviations: AE, proaerolysin; APC, allophycocyanin; CFU, colony-forming unit; iPS, induced pluripotent stem cell.