Skip to main content
. Author manuscript; available in PMC: 2017 Dec 1.
Published in final edited form as: Stem Cells. 2016 Sep 1;34(12):2916–2929. doi: 10.1002/stem.2471

Figure 7.

Figure 7

p53 regulates cardiogenic gene activation in HDAC1-depleted CMCs. (A): Real-time qPCR evaluating the expression of p53 in CMCs 72 h after transduction with NT control, HDAC1, HDAC4, HDAC7, p53, or HDAC1 and p53 shRNA constructs. Values are mean (n=4 patient samples) ± SEM. * P <0.05 (Relative to NT shRNA) and † P <0.05 (Relative to shHDAC1). (B): Representative immunoblots detecting p53 and acetylated p53 (Acetyl-p53; acetylated lysine 382) in total protein extracts derived from CMCs 72 h after infection with NT control, HDAC1, HDAC4, or HDAC7 shRNA lentiviral vectors. (C-F): Real-time qPCR assessing the expression of stemness-, cardiac-, smooth muscle- or endothelial-lineage specific transcripts, respectively, in CMCs transduced with NT control, HDAC1, or p53 and HDAC1 shRNA constructs. Values are mean (n=4) ± SEM. * P <0.05 (Relative to NT-shRNA) and † P <0.05 (Relative to shHDAC1). (G): Real-time qPCR quantifying the expression of HDAC1 in CMCs transduced with NT control, HDAC1, or p53 and HDAC1 shRNA constructs. Values are mean (n=4) ± SEM. * P <0.05 (Relative to NT shRNA). (H): Representative immunoblots detecting p53 (n=3), p21 (n=2), acetylated p53 (n=3), and Mef2C (n=3) in protein extracts isolated from NT control, HDAC1, or HDAC1 and p53 shRNA transduced CMCs.