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Updated: Jul 1, 2026

Sequential In vivo Imaging of Osteogenic Stem/Progenitor Cells During Fracture Repair
Published on: May 23, 2014
MYLK-AS1 improves fracture by targeting miR-146a-5p to regulate cell viability and apoptosis in osteoblasts
Wuluhan Mahan1, Haoze Gao2, Ning Liu3
1Department of Orthopedic Trauma, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830011, China.
Background:
Delayed fracture healing (DFH) is a significant burden for patients. Therefore, early diagnosis and detection are important for the treatment of DFH. The long non-coding RNA (LncRNA) MYLK-AS1 is abnormally expressed in patients with DFH and has the potential to be used as a diagnostic marker.
Methods:
40 patients with DFH and 87 patients with normal fracture healing were included. The levels of MYLK-AS1, miR-146a-5p and several mRNA markers of osteogenic differentiation were assessed by RT-qPCR. The diagnostic value of MYLK-AS1, miR-146a-5p was assessed using ROC curves. Cell proliferation ability was assessed by CCK-8, and apoptosis rate was detected by flow cytometry. DLR, RIP and RNA pull down assays demonstrated the targeting relationship between MYLK-AS1 and miR-146a-5p.
Results:
MYLK-AS1 levels were significantly lower and miR-146a-5p levels were significantly up-regulated in DFH compared to normal healing patients. MYLK-AS1 was found to target miR-146a-5p, and the levels were negatively correlated with each other. MYLK-AS1 with miR-146a-5p is of high value for the diagnosis of DFH. High expression of MYLK-AS1 could inhibit miR-146a-5p levels, support cell proliferation, reduce apoptosis, and increase the levels of osteogenesis-specific matrix proteins and osteogenesis-related regulatory factors.
Conclusion:
MYLK-AS1 has potential as a diagnostic marker for DFH. By increasing the expression level of MYLK-AS1 in cells can reduce the level of miR-146a-5p, increase the activity of osteoblasts and reduce their apoptosis rate, thus affecting the process of fracture healing.
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