Effect of miR-654-3p targeting EMP1 on osteoblast activity and differentiation in delayed fracture healing.

miR-654-3p靶向EMP1对延迟骨折愈合中成骨细胞活性和分化的影响

阅读:17
作者:Wang Shantao, Wang Mingwei, Sun Shengliang, Liu Xinsheng, Li Danzhi
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.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。