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Updated: Jun 25, 2026

Sequential In vivo Imaging of Osteogenic Stem/Progenitor Cells During Fracture Repair
Published on: May 23, 2014
Effect of miR-654-3p targeting EMP1 on osteoblast activity and differentiation in delayed fracture healing
Shantao Wang1, Mingwei Wang2, Shengliang Sun3
1Spinal Trauma Orthopedics, Yidu Central Hospital of Weifang, No.5168, Jiangjunshan Road, Qingzhou, Weifang, 262500, China. wangshantaodr@163.com.
Background:
Delayed fracture healing (DFH) is a common postoperative complication in fracture patients, and a validated serum marker may aid in the clinical management and improve the prognosis of fracture patients. In this study, we investigated the diagnostic role and potential regulatory mechanisms of miR-654-3p in DFH.
Methods:
73 patients with DFH and 75 patients with normal fracture healing (NFH) were included. Expression of miR-654-3p and EMP1 and several mRNA markers of osteogenic differentiation were evaluated by RT-qPCR. The diagnostic value of miR-654-3p and EMP1 alone and in combination was assessed using ROC curves. Cell proliferation capacity was assessed by CCK-8 and apoptosis rate by flow cytometry. DLR experiments demonstrated the targeting relationship between miR-654-3p and EMP1.
Results:
Levels of miR-654-3p were found to be significantly lower in DFH compared to NFH. Following cell differentiation treatment, miR-654-3p levels increased and EMP1 levels decreased. Furthermore, a negative correlation was identified between miR-654-3p and EMP1 target binding and expression levels. The combination of miR-654-3p and EMP1 holds significant diagnostic value for DFH. miR-654-3p high expression can inhibit EMP1 levels, which promotes cell proliferation, increases osteoblast activity and levels of differentiation markers, and decreases the rate of apoptosis.
Conclusion:
miR-654-3p and EMP1 are aberrantly expressed in DFH, and both have high diagnostic value for DFH. miR-654-3p is involved in the proliferation, differentiation, and apoptotic activities of osteoblasts by regulating the level of EMP1, thus affecting the progression of DFH.
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