Suppr超能文献

环状RNA_0005918通过吸附微小RNA_622加重椎间盘退变

Circ_0005918 Sponges miR-622 to Aggravate Intervertebral Disc Degeneration.

作者信息

Cui Yan, Zhao Xintong, Wu Yangang

机构信息

Department of Orthopaedics, the Hospital of Shunyi District, Beijing, China.

出版信息

Front Cell Dev Biol. 2022 Jul 8;10:905213. doi: 10.3389/fcell.2022.905213. eCollection 2022.

Abstract

Intervertebral discdegeneration (IDD) is the most common cause of lower back pain, but the exact molecular mechanism of IDD is still unknown. Recently, studies have shown that circular RNAs (circRNAs) regulate diverse biological procedures such as cell metastasis, growth, metabolism, migration, apoptosis, and invasion. We demonstrated that IL-1β and TNF-α induced circ_0005918 expression in the NP cell, and circ_0005918 was overexpressed in the IDD group compared with the control group. Moreover, the upregulated expression of circ_0005918 was associated with disc degeneration degree. The elevated expression of circ_0005918 promoted cell growth and ECM degradation, and it induced secretion of inflammatory cytokines including IL-1β, IL-6, and TNF-α. Moreover, we found that circ_0005918 sponged miR-622 in the NP cell. In addition, the exposure to IL-1β and TNF-α suppressed the expression of miR-622, which was downregulated in the IDD group compared with the control group. Furthermore, the downregulated expression of miR-622 was associated with disc degeneration degree. The expression level of miR-622 was negatively associated with circ_0005918 expression in the IDD group. In conclusion, circ_0005918 regulated cell growth, ECM degradation, and secretion of inflammatory cytokines by regulating miR-622 expression. These data suggested that circ_0005918 played important roles in the development of IDD via sponging miR-622.

摘要

椎间盘退变(IDD)是下腰痛最常见的原因,但IDD的确切分子机制仍不清楚。最近,研究表明环状RNA(circRNAs)可调节多种生物学过程,如细胞转移、生长、代谢、迁移、凋亡和侵袭。我们证明白细胞介素-1β(IL-1β)和肿瘤坏死因子-α(TNF-α)可诱导髓核细胞中circ_0005918的表达,与对照组相比,IDD组中circ_0005918过表达。此外,circ_0005918的表达上调与椎间盘退变程度相关。circ_0005918表达升高促进细胞生长和细胞外基质(ECM)降解,并诱导包括IL-1β、IL-6和TNF-α在内的炎性细胞因子分泌。此外,我们发现circ_0005918在髓核细胞中可吸附miR-622。另外,暴露于IL-1β和TNF-α会抑制miR-622的表达,与对照组相比,IDD组中miR-622表达下调。此外,miR-622的表达下调与椎间盘退变程度相关。在IDD组中,miR-622的表达水平与circ_0005918的表达呈负相关。总之,circ_0005918通过调节miR-622的表达来调控细胞生长、ECM降解和炎性细胞因子分泌。这些数据表明circ_0005918通过吸附miR-622在IDD的发生发展中起重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27dd/9304550/f557f60ccaf5/fcell-10-905213-g001.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验