Surprisingly, compared with the empty vector and control groups (p < 0.05; Figures 2D,I,K), PBX1 overexpression down-regulated DNA repair-related protein expression (89 and 116 kDa PARP1, Ku 70, Ku 80, Rad51, and PAR) (p < 0.05; Figures 2D,K,L), suggesting that DNA damage reduction rather than DNA repair may be the major, if not unique, mechanism underlying the attenuation of cellular senescence and apoptosis in HF-MSCs by PBX1. Here, PBX1 is linked to hydrops fetalis.