miR‐5701 Drives Bone Fracture Repair in Osteoporosis Through TP53 Regulation

This study identified miR-5701 and TP53 through bioinformatics analysis utilizing the GEO, GeneCards, and miRDB databases. The serum expression levels were quantified via Reverse Transcription Quantitative Real-time Polymerase Chain Reaction (RT-qPCR). The binding relationship between miR-5701 and TP53 was confirmed using dual luciferase reporter assays. Subsequently, MC3T3-E1 cell differentiation was induced with Bone Morphogenetic Protein 2 (BMP2), and the expression changes of miR-5701 and TP53 after cell differentiation were detected. Subsequently, after overexpression of miR-5701 and TP53, the expression levels of key osteogenic differentiation markers Alkaline Phosphatase (ALP), Osteocalcin (OCN), and type I collagen were evaluated by ELISA. Serum miR-5701 expression is downregulated in osteoporotic fracture patients, while it increases after osteoblast differentiation. TP53 is a negative regulatory binding factor downstream of miR-5701. The mRNA expression of TP53 in the patient serum and the differentiated osteoblast cells is exactly opposite to that of miR-5701. Overexpression of miR-5701-mediated promotion of osteoblast proliferation and differentiation can be reversed by TP53. miR-5701 was found to facilitate osteoblast proliferation and differentiation through negative regulation of the target gene TP53 expression, suggesting that miR-5701 could serve as a promising therapeutic target for promoting fracture healing.