Transient p53 Suppression Increases Reprogramming Efficiency without Affecting Apoptosis and DNA Damage
Flow cytometry of normal human dermal fibroblasts (NHDFs) on days 0, 7, 14, 21, and 28 after reprogramming with the episomal plasmids hOCT4, hSOX2, hKLF4, hL-MYC, and hLIN28 (hOSKUL) with or without (w/wo) a short hairpin to p53 (shp53).
(A–E) Flow cytometry was performed with (A) the pluripotency markers SSEA4 and TRA1-60, (B) the tumor suppressor p53, (C) the cell-cycle regulator p21, (D) the proapoptotic marker PUMA, and (E) the double-stranded DNA damage marker H2A.X.
(F) Overview depicting the mechanisms involved in transient p53 suppression during reprogramming. Y error bars depict SD of three independent experiments. ∗p < 0.05. See also Figure S2.