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. Author manuscript; available in PMC: 2019 Aug 1.
Published in final edited form as: Stem Cell Rev. 2018 Aug;14(4):612–625. doi: 10.1007/s12015-018-9815-z

Figure 1. P16INK4A expression is associated with the aging/senescence of cardiac progenitor cells.

Figure 1

Representative images showed the senescence-associated β-galactosidase staining in hCPCs from patients at the age of 44 years old (A), 71 years old (B), and 93 years old (C). D. Quantitative analysis of total β-galactosidase staining. E. Multiple lines of hCPCs showed variation in population doubling times as measured by CyQuant and viability assay cell counts from different groups of patients (n=3 independent experiments). See the Supplemental Table S2 for the basic demographic information for the cardiac tissue donors. F. Differences in proliferation rates were observed in three different hCPC groups (n=3 lines of hCPCs per group). G. Real time qPCR data showed the p16INK4A gene expression in hCPCs from different groups of patients (n=3 independent experiments). * indicates p<0.05 versus the group of hCPCs-Y for panel E, F, G. H. Quantitative analysis of Western blot showing the significant increase of p16INK4A expression in the group of hCPCs-A versus the group of hCPCs-Y at passage 6 (P6) (n=3 lines of hCPCs per group). I. Quantitative analysis of Western blot revealed an increase in p16INK4A protein after replicative passaging (P15 versus P6) of three lines of hCPCs in the hCPCs-Y group. J. Quantitative analysis of Western blot showed an increase in p16INK4A protein expression in three lines of hCPCs at passage 6 (P6) in the hCPCs-Y group following induction of stress-induced premature senescence through treatment in 0.5 μM doxorubicin for 18 h. * indicates p<0.05. All data were presented as means ± SD from either 3 independent experiments or 3 lines of hCPCs per group.