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 4. p53 contribute to impaired osteogenesis of BMMSCs via inhibiting the transcription of miR-17-92 cluster. BMMSCs 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-C) Real-time PCR analyses for the expression of miR-17, miR-18a, miR-19a, miR-19b, miR-20a and miR-92a in bone (A), bone marrow (B) and BMMSCs (C) of young and old mice. Normalization to ß-actin. (D-F) Real-time PCR and western blot analysis of p53 (D, E) and real-time PCR of miR-17 (F) expression in BMMSCs derived from young and old mice after osteogenic differentiation for 7 d. Normalization to ß-actin and U6. (G) Pri-miR-17 transcript analysis by Taqman-based qPCR. Normalization to GAPDH. (H) Real-time PCR analysis of the mature miR-17-92 cluster after upregulating P53 for 48 h. Normalization to U6.