miR-551a promotes osteogenic differentiation of BMSCs by regulating SKI.

Background

MiR-551a has been implicated in various biological processes, but its role in fracture healing remains unclear. This study aimed to investigate the role of miR-551a in fracture healing.

Objective

This study is intended to examine the regulatory role of miR-551a in fracture healing through its interaction with SKI.

Methods

The osteogenic differentiation potential of human bone marrow-derived mesenchymal stem cells (hBMSCs) was assessed through quantification of alkaline phosphatase activity using a commercial alkaline phosphatase (ALP) assay kit and measurement of osteogenic marker gene expression levels, including Osteocalcin (OCN), Runt-related transcription factor 2 (RUNX2), and Collagen I via RT-qPCR and Western blot experiments. dual-luciferase reporter assay was utilized to examine the regulatory interaction between miR-551a and SKI.

Results

Serum levels of miR-551a were significantly elevated in treated fracture patients. Functional analysis revealed that miR-551a overexpression enhanced ALP activity and elevated expression of osteogenic markers, whereas miR-551a inhibition reduced ALP activity and downregulated these markers; SKI knockdown reversed the inhibitory effects of miR-551a suppression. Mechanistically, miR-551a directly targets and negatively regulates SKI.

Conclusions

In vitro evidence suggests that miR-551a may promote osteogenic differentiation of hBMSCs by directly targeting and downregulating SKI, which may be relevant to fracture repair.