| 王云浩,孙中仪,于召龙,李秋园,朱文峰,田纪伟.Linc01776在椎间盘退行性变中生物学功能的研究[J].,2019,19(18):3405-3409 |
| Linc01776在椎间盘退行性变中生物学功能的研究 |
| The Biological Function Analysis of Linc01776 in the Degeneration of Intervertebral Disc |
| 投稿时间：2019-04-11 修订日期：2019-05-06 |
| DOI：10.13241/j.cnki.pmb.2019.18.002 |
| 中文关键词: 椎间盘退行性变 长链非编码RNA linc01776 竞争性内源RNA |
| 英文关键词: Intervertebral disc degeneration Long non-coding RNA Linc01776 Competitive endogenous RNA |
| 基金项目:国家自然科学基金项目（81572169） |
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| 中文摘要: |
| 摘要 目的：椎间盘退行性变（intervertebral disc degeneration, IVDD）是中老年人中的高发病率与高致残率的疾病，目前其病理生理机制尚未完全研究清楚。本实验旨在研究linc01776在IVDD中的差异性表达，并通过生物信息学探索调控IVDD的分子学机制，从而为IVDD的治疗提供作用靶点。方法：根据Pffirrmann评分，将退变椎间盘标本分成对照组与IVDD组，通过qRT-PCR验证linc01776在退变椎间盘中的差异表达；构建Linc01776敲除质粒表达载体，并研究Linc01776在IVDD中生物功能学研究；预测Linc01776参与的竞争性内源RNA（CeRNA）调控机制。结果：linc01776在退变椎间盘中表达显著增加。敲除linc01776后，Aggrecan表达增加，MMP3、MMP13表达减少，细胞外基质分解降低。通过生物信息学预测Linc01776/miR-196b-5p/Akt1的CeRNA机制调控通路。结论：Linc01776促进髓核细胞外基质降解，调控IVDD的发生与发展。Linc01776/miR-196b-5p/Akt1信号轴可能为其调控IVDD进程的CeRNA机制调控通路。 |
| 英文摘要: |
| ABSTRACT Objective: Intervertebral disc degeneration (IVDD) is a disease with high morbidity and high disability in middle-aged and elderly people. The pathophysiological mechanism has not been fully studied. This study investigated the differential expression of linc01776 in IVDD and explored the molecular mechanism of IVDD through bioinformatics. This may provid a target for the treatment of IVDD. Methods: According to Pffirrmann score, degenerative disc tissues were divided into control group and IVDD group and qRT-PCR was used to verify the differential expression of linc01776 in degenerated intervertebral discs. The Linc01776 knocking-out plasmid expression vector was constructed to study the biofunctionality of Linc01776 in IVDD. The competitinge endogenous RNA (CeRNA) regulatory mechanism involved in Linc01776 was predicted. Results: The expression of linc01776 was significantly increased in the degenerated intervertebral disc. Knocking out linc01776 could promote the expression of Aggrecan and inhabit the expression of the MMP3 and MMP13. What's more, it could further promote the decomposition of extracellular matrix. The regulatory pathway of the CeRNA mechanism of Linc01776/miR-196b-5p/Akt1 was predicted by bioinformatics. Conclusion: Linc01776 promotes the degradation of nucleus pulposus extracellular matrix and regulates the occurrence and development of IVDD. The Linc01776/miR-196b-5p/Akt1 signal axis may be a regulatory pathway for the CeRNA mechanism that regulates IVDD progression. |
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