Yuanming Luo, Qingfeng Zhang, Changqing Shao, Jin Li, Jiaojiao Chen, Liang Han, Xiaowei Jiang, Li Hong
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引用次数: 0
Abstract
Background: Osteoporotic fractures (OPF) have a serious impact on the health of patients. It is of great importance to investigate the diagnostic effect of SNH16 on OPF and the mechanism of action to promote fracture healing.
Methods: 132 OPF patients and 128 OP patients were included. The levels of SNHG16, Col I, RUNX2 and OCN were evaluated by RT-qPCR. The diagnostic value of SNHG16 was evaluated by ROC curve. Cell proliferation ability was assessed by CCK-8, and apoptosis rate was detected by flow cytometry. ENCORI was used to predict the binding sites of SNHG16 with downstream target genes. DLR assay demonstrated the targeting relationship between SNHG16 and miR-432-5p.
Results: SNHG16 was poorly expressed in OPF patients compared with OP patients, and its expression was lower in patients with delayed healing. In addition, in the OPF, OPG level was decreased, the level of RANKL was increased, and the balance of bone resorption formation is disrupted leading to fractures. Knockdown of SNHG16 results in decreased cell proliferation and increased apoptosis, and high SNHG16 expression decreases miR-432-5p expression, thereby increasing the levels of Col I, RUNX2 and OCN.
Conclusion: Increasing SNHG16 can reduce the level of miR-432-5p thereby increasing the level of osteosynthesis proteins and restoring cellular activity, thereby promoting fracture healing.
HereditasBiochemistry, Genetics and Molecular Biology-Genetics
CiteScore
3.80
自引率
3.70%
发文量
0
期刊介绍:
For almost a century, Hereditas has published original cutting-edge research and reviews. As the Official journal of the Mendelian Society of Lund, the journal welcomes research from across all areas of genetics and genomics. Topics of interest include human and medical genetics, animal and plant genetics, microbial genetics, agriculture and bioinformatics.