Suppr超能文献

微小RNA-181a通过靶向骨关节炎中的3-磷酸甘油脱氢酶1样蛋白(GPD1L)调节软骨细胞凋亡。

miR-181a Modulates Chondrocyte Apoptosis by Targeting Glycerol-3-Phosphate Dehydrogenase 1-Like Protein (GPD1L) in Osteoarthritis.

作者信息

Zhai Xicheng, Meng Ru, Li Hongbiao, Li Jie, Jing Lei, Qin Lei, Gao Yulei

机构信息

Department of Orthopedics, Shanxian Central Hospital, Heze, Shandong, China (mainland).

Department of Orthopedics, The 88th Hospital of PLA, Taian, Shandong, China (mainland).

出版信息

Med Sci Monit. 2017 Mar 10;23:1224-1231. doi: 10.12659/msm.899228.

Abstract

BACKGROUND miR-181a is a small non-coding RNA known to be dysregulated in osteoarthritis (OA), but the role of miR-181a in human OA remains unclear. The aim of this study was to identify its function and molecular target in chondrocytes during OA pathogenesis. MATERIAL AND METHODS The function of miR-181a was assessed by gain-of-function studies in human OA chondrocytes. Potential targets of miR-181a were predicted using series of bioinformatics and intersection analysis, then confirmed by luciferase reporter assay. Gene expression was quantified using quantitative reverse transcription PCR (qRT-PCR) assays, and protein production was quantified by Western blot analysis. RESULTS The FITC apoptosis assay results indicated that the upregulation of miR-181a led to an increase of apoptosis rate in chondrocytes. Then bioinformatic analysis identified potential target sites of the miR-181a located in the 3' untranslated region of GPD1L. Dual-luciferase reporter assays results showed that GPD1L is a target gene of miR-181a. Furthermore, Western blot and qRT-PCR analysis demonstrated that miR-181a inhibited GPD1L gene expression. Increased GPD1L and decreased miRNA-181a were observed in tissues from osteoarthritis patients. Moreover, we found a highly negative correlation between miRNA-181a and GPD1L. CONCLUSIONS Our results demonstrated that miR-181a may play an important role in the pathogenesis of OA through targeting GPD1L and regulating chondrocyte apoptosis.

摘要

背景

miR-181a是一种已知在骨关节炎(OA)中表达失调的小非编码RNA,但miR-181a在人类OA中的作用仍不清楚。本研究的目的是确定其在OA发病机制中软骨细胞的功能和分子靶点。

材料与方法

通过在人类OA软骨细胞中进行功能获得性研究来评估miR-181a的功能。使用一系列生物信息学和交集分析预测miR-181a的潜在靶点,然后通过荧光素酶报告基因测定进行确认。使用定量逆转录PCR(qRT-PCR)测定法对基因表达进行定量,并通过蛋白质印迹分析对蛋白质产生进行定量。

结果

FITC凋亡检测结果表明,miR-181a的上调导致软骨细胞凋亡率增加。然后生物信息学分析确定了位于GPD1L 3'非翻译区的miR-181a潜在靶位点。双荧光素酶报告基因测定结果表明GPD1L是miR-181a的靶基因。此外,蛋白质印迹和qRT-PCR分析表明miR-181a抑制GPD1L基因表达。在骨关节炎患者的组织中观察到GPD1L增加而miRNA-181a减少。此外,我们发现miRNA-181a与GPD1L之间存在高度负相关。

结论

我们的结果表明,miR-181a可能通过靶向GPD1L并调节软骨细胞凋亡在OA发病机制中发挥重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6276/5360418/d0ab9183a5ac/medscimonit-23-1224-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