TUG1 knockdown promoted viability and inhibited apoptosis and cartilage ECM degradation in chondrocytes via the miR-17-5p/FUT1 pathway in osteoarthritis.
TUG1 knockdown promoted viability and inhibited apoptosis and cartilage ECM degradation in chondrocytes via the miR-17-5p/FUT1 pathway in osteoarthritis.
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DOI：
10.3892/etm.2020.9283
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发表时间：
2020-12
影响因子：
2.7
通讯作者：
Yang J
中科院分区：
文献类型：
--
作者：
Li Z;Wang J;Yang J
骨关节炎（OA）是一种以软骨破坏为特征的退行性疾病。先前的研究已经证明，长的非编码RNA在OA进展中起作用。本研究旨在探讨牛磺酸上调基因（TUG）1在OA中的作用及其机制。逆转录定量PCR结果显示TUG 1在OA软骨组织和白细胞介素1 β诱导的软骨细胞中表达增加。细胞计数试剂盒-8和流式细胞仪分析显示，TUG 1敲低促进细胞活力和抑制细胞凋亡。Western blotting检测软骨细胞基质金属蛋白13（MMP 13）、Ⅱ型胶原和聚集蛋白聚糖（aggrecan）的表达，结果显示TUG 1基因敲低可显著降低IL-1β刺激的软骨细胞MMP 13的表达，增加Ⅱ型胶原和聚集蛋白聚糖的表达，表明细胞外基质（ECM）损伤受到抑制。此外，使用生物信息学分析、双荧光素酶报告基因和RNA免疫沉淀试验，发现TUG 1通过靶向miR-17- 5 p上调岩藻糖基转移酶（FUT）1。此外，在OA软骨组织和IL-1β诱导的软骨细胞中，miR-17- 5 p下调，FUT 1上调。TUG 1过表达逆转了IL-1β激活的软骨细胞中miR-17- 5 p介导的细胞活力、细胞凋亡和ECM降解的上述作用。此外，FUT 1敲低对FUT 1敲低介导的细胞活力、凋亡和ECM降解的影响可通过miR-17- 5 p抑制逆转。总之，TUG 1敲低通过miR-17- 5 p下调FUT 1抑制OA进展。
Osteoarthritis (OA) is a degenerative disease characterized by cartilage destruction. Previous research has demonstrated that long non-coding RNAs serve a role in OA progression. The current study aimed to determine the function and mechanism of taurine upregulated gene (TUG) 1 in OA. The results of reverse transcription quantitative PCR revealed that TUG1 was elevated in OA cartilage tissues and interleukin (IL)-1β-induced chondrocytes. Cell Counting kit-8 and flow cytometry analysis revealed that TUG1 knockdown promoted cell viability and inhibited cell apoptosis. Furthermore, matrix metalloprotein (MMP) 13, collagen II and aggrecan expression was determined by western blotting, of which the results demonstrated that TUG1 knockdown significantly decreased MMP13 expression and increased collagen II and aggrecan expression in IL-1β-stimulated chondrocytes, indicating that extracellular matrix (ECM) damage was inhibited. Additionally, using bioinformatics analysis, dual-luciferase reporter and RNA immunoprecipitation assays, TUG1 was revealed to upregulate fucosyltransferase (FUT) 1 by targeting miR-17-5p. Furthermore, miR-17-5p was downregulated and FUT1 upregulated in OA cartilage tissues and IL-1β-induced chondrocytes. TUG1 overexpression reversed the aforementioned effects on cell viability, cell apoptosis and ECM degradation mediated by miR-17-5p in IL-1β-activated chondrocytes. Additionally, the effects of FUT1 knockdown on cell viability, apoptosis and ECM degradation mediated by FUT1 knockdown were reversed by miR-17-5p inhibition. In conclusion, TUG1 knockdown inhibited OA progression by downregulating FUT1 via miR-17-5p.
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影响因子：
3.8
作者：
Li J;Lai Y;Ma J;Liu Y;Bi J;Zhang L;Chen L;Yao C;Lv W;Chang G;Wang S;Ouyang M;Wang W
通讯作者：
Wang W
影响因子：
37.3
作者：
Huang MD;Chen WM;Qi FZ;Sun M;Xu TP;Ma P;Shu YQ
通讯作者：
Shu YQ
癌胎儿 miR-17-5p 表达升高通过抑制其靶基因 P130 调节结直肠癌进展
影响因子：
16.6
作者：
Ma, Yanlei;Zhang, Peng;Qin, Huanlong
通讯作者：
Qin, Huanlong
DOI：
10.1016/j.biocel.2017.12.003
发表时间：
2018-01-01
影响因子：
4
作者：
Hu, Jialei;Wang, Zi;Jia, Li
通讯作者：
Jia, Li
MicroRNA-193b-3p 通过靶向 HDAC3 调节软骨形成和软骨细胞代谢
影响因子：
12.4
作者：
Meng F;Li Z;Zhang Z;Yang Z;Kang Y;Zhao X;Long D;Hu S;Gu M;He S;Wu P;Chang Z;He A;Liao W
通讯作者：
Liao W