Fig. 4: SAA-iPSC exhibit deficient telomere elongation during reprogramming and telomere shortening upon hematopoietic differentiation | Cell Death & Disease

Fig. 4: SAA-iPSC exhibit deficient telomere elongation during reprogramming and telomere shortening upon hematopoietic differentiation

From: iPSC modeling of severe aplastic anemia reveals impaired differentiation and telomere shortening in blood progenitors

Fig. 4

a Analysis of telomere length in parental fibroblasts (dark grey bars) and iPSC passage 30 (light blue bars) and 50 (green bars) in WT controls and SAA cell lines. One-way ANOVA with Tukey’s multiple comparison test was used for statistical comparison between fibroblasts and iPSC passage 30 and passage 50 (*p < 0.05); b Analysis of telomere length in iPSC passage 50 (green bars) and iPSC-based hematopoietic progenitors (HPC) differentiated from iPSC passage 50 (light grey bars) in WT controls and SAA cell lines. Multiple t-test using Holm-Sidak method was used for statistical comparison between iPSC passage 50 and HPC; c Analysis of telomerase activity in parental fibroblasts (dark grey bars) and iPSC at passage 30 (light blue bars) and 50 (green bars) in WT controls and SAA cell lines. One-way ANOVA with Tukey’s multiple comparison test was used for statistical comparison between fibroblasts and iPSC passage 30 and passage 50; d Analysis of telomerase activity in iPSC passage 50 (green bars) and iPSC-based hematopoietic progenitors (HPC) differentiated from iPSC passage 50 (light grey bars) in WT and SAA cell lines. Multiple t-test using Holm–Sidak method was used for statistical comparison between iPSC passage 50 and HPC. a–d data is presented as mean of at least 3 independent experiments ± S.E.M. Data for all control cell lines is averaged in one group (WT)

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