SATB1 promotes osteogenic differentiation of diabetic rat BMSCs through MAPK signalling activation

OBJECTIVE: Special AT-rich binding protein 1 (SATB1), a chromatin organizer and global transcriptional regulator, plays an important role in tumorigenesis and immune response. However, its function in the osteogenic differentiation of bone marrow-derived mesenchymal stem cells (BMSCs) remains unknown. Therefore, this study aimed to explore the role of SATB1 in osteogenesis. METHODS: BMSCs were collected from the type 2 diabetes rat model and the protein and gene expression of SATB1 and osteospecific genes were evaluated post osteogenic induction. RESULTS: SATB1 protein expression significantly decreased in diabetic rat BMSCs whereas it increased in BMSCs following osteogenic induction. SATB1 knockdown significantly suppressed the expression of osteospecific genes, including alkaline phosphatase (Alp), runt-related transcription factor 2, and osteocalcin, and reduced the number of mineral deposits and ALP activity, whereas SATB1 overexpression yielded the opposite results. Moreover, SATB1 knockdown suppressed activation of the MAPK signalling pathway (phosphorylation of p38 and ERK), and MAPK pathway inhibitors could reverse the inhibitory effect of SATB1 knockdown on osteogenic differentiation of BMSCs. CONCLUSION: SATB1 plays a key role in the osteogenic differentiation of BMSCs via the p38 MAPK and ERK MAPK signalling pathways. These findings may provide a new strategy for the application of BMSCs in bone regeneration.