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


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.