Research Paper Volume 7, Issue 3 pp 205—216

The p53/miR-17/Smurf1 pathway mediates skeletal deformities in an age-related model via inhibiting the function of mesenchymal stem cells

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Figure 3.

Overexpression of p53 changed the phenotype of young BMMSCs into old BMMSCs. BMMSCs from young mice were lentivirally transduced to upregulate the expression level of p53 (= pLenti-p53) or were transduced as lentiviral control (= pLenti-Cont). Statistically analyzed values show the mean ± SD (n=10). * p < 0.05. (A) Alizarin red staining of pLenti-p53 and of pLenti-Cont after osteogenic inducing for 14 days. Cont = Control, OS = osteogenically induced. The values show the mean ± SD (n=10). * p < 0.05. (B-C) Real-time PCR and western blot analyses on BMMSCs with lentiviral transduction (pLenti-p53 and pLenti-Cont) and with/without osteogenic induction for the osteogenic markers Runx2, ALP, osterix. Normalization to ß-actin. (D-E) Histological analyses and corresponding statistical analysis of tissue sections from subcutaneous pockets on the backs of 6-week-old NOD/SCID mice with implanted HA/TCP ceramic particles mixed with BMMSCs from young mice with lentiviral transduction of p53 and control.