Journal of orthopaedic surgery and research · 2025
MYLK-AS1 improves fracture by targeting miR-146a-5p to regulate cell viability and apoptosis in osteoblasts.
СтатьяНазвание и аннотация: Перевод в очереди
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Mahan Wuluhan, Gao Haoze, Liu Ning, Zhao Zhenyu, Huang Yingxuan
Аннотация
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.
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.