长链非编码RNA SNHG16对骨质疏松性骨折的诊断价值及其对骨折愈合的潜在调控作用

Diagnostic value of LncRNA SNHG16 for osteoporotic fractures and its potential regulation of fracture healing.

作者信息

Luo Yuanming, Zhang Qingfeng, Shao Changqing, Li Jin, Chen Jiaojiao, Han Liang, Jiang Xiaowei, Hong Li

机构信息

Department of Orthopedics, The Affiliated Hospital of Jiaxing University, Jiaxing, 314001, China.

Department of Spine, Beijing University of Chinese Medicine Third Affiliated Hospital, Beijing, 100029, China.

出版信息

Hereditas. 2025 Apr 7;162(1):54. doi: 10.1186/s41065-025-00423-6.

DOI:10.1186/s41065-025-00423-6

PMID:40197315

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11974092/

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.

摘要

背景

骨质疏松性骨折（OPF）对患者健康有严重影响。研究SNHG16对OPF的诊断作用及促进骨折愈合的作用机制具有重要意义。

方法

纳入132例OPF患者和128例骨质疏松症（OP）患者。采用RT-qPCR检测SNHG16、I型胶原（Col I）、 runt相关转录因子2（RUNX2）和骨钙素（OCN）水平。通过受试者工作特征（ROC）曲线评估SNHG16的诊断价值。采用细胞计数试剂盒-8（CCK-8）评估细胞增殖能力，通过流式细胞术检测细胞凋亡率。利用ENCORI预测SNHG16与下游靶基因的结合位点。双荧光素酶报告基因实验（DLR）验证SNHG16与miR-432-5p的靶向关系。

结果

与OP患者相比，OPF患者中SNHG16表达较低，且在愈合延迟患者中其表达更低。此外，在OPF中，骨保护素（OPG）水平降低，核因子κB受体活化因子配体（RANKL）水平升高，骨吸收与骨形成平衡被破坏导致骨折。敲低SNHG16导致细胞增殖减少和凋亡增加，高表达SNHG16降低miR-432-5p表达，从而增加Col I、RUNX2和OCN水平。