Knocking-down long non-coding RNA LINC01094 prohibits chondrocyte apoptosis via regulating microRNA-577/metal-regulatory transcription factor 1 axis.

IF 1.6 4区 医学
Feiri Huang, Zhongliang Su, Jie Yang, Xizhen Zhao, Yaozeng Xu
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引用次数: 0

Abstract

Purpose: The abnormal function and survival of chondrocytes result in articular cartilage failure, which may accelerate the onset and development of osteoarthritis (OA). This study is aimed to investigate the role of LINC01094 in chondrocyte apoptosis.

Methods: The viability and apoptosis of lipopolysaccharide (LPS)-induced chondrocytes were evaluated through CCK-8 assay and flow cytometry analysis, respectively. The expression levels of LINC01094, miR-577 and MTF1 were detected by qRT-PCR. Dual luciferase reporter tests were implemented for the verification of targeted relationships among them. Western blotting was employed to measure the levels of pro-apoptotic proteins (Caspase3 and Caspase9).

Results: The viability of LPS-induced chondrocytes was overtly promoted by loss of LINC01094 or miR-577 upregulation, but could be repressed via MTF1 overexpression. The opposite results were observed in apoptosis rate and the levels of Caspase3 and Caspase9. LINC01094 directly bound to miR-577, while MTF1 was verified to be modulated by miR-577. Both LINC01094 and MTF1 were at high levels, whereas miR-577 was at low level in OA synovial fluid and LPS-induced chondrocytes. Furthermore, the highly expressed miR-577 abolished the influences of MTF1 overexpression on LPS-induced chondrocytes.

Conclusions: Silencing of LINC01094 represses the apoptosis of chondrocytes through upregulating miR-577 expression and downregulating MTF1 levels, providing a preliminary insight for the treatment of OA in the future.

敲除长非编码RNA LINC01094可通过调节microRNA-577/金属调节转录因子1轴阻止软骨细胞凋亡
目的:软骨细胞的功能和存活异常会导致关节软骨功能衰竭,从而加速骨关节炎(OA)的发生和发展。本研究旨在探讨 LINC01094 在软骨细胞凋亡中的作用:方法:通过 CCK-8 检测法和流式细胞术分析法分别评估脂多糖(LPS)诱导的软骨细胞的活力和凋亡。通过 qRT-PCR 检测 LINC01094、miR-577 和 MTF1 的表达水平。为了验证它们之间的靶向关系,还进行了双荧光素酶报告试验。采用 Western 印迹法测定促凋亡蛋白(Caspase3 和 Caspase9)的水平:结果:LINC01094的缺失或miR-577的上调明显促进了LPS诱导的软骨细胞的活力,但MTF1的过表达则抑制了软骨细胞的活力。在细胞凋亡率以及 Caspase3 和 Caspase9 水平方面观察到了相反的结果。LINC01094 直接与 miR-577 结合,而 MTF1 则被证实受 miR-577 调节。在 OA 滑液和 LPS 诱导的软骨细胞中,LINC01094 和 MTF1 均处于高水平,而 miR-577 则处于低水平。此外,高表达的 miR-577 可消除 MTF1 过表达对 LPS 诱导的软骨细胞的影响:结论:沉默LINC01094可通过上调miR-577的表达和下调MTF1的水平抑制软骨细胞的凋亡,这为未来治疗OA提供了初步启示。
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来源期刊
自引率
0.00%
发文量
91
期刊介绍: Journal of Orthopaedic Surgery is an open access peer-reviewed journal publishing original reviews and research articles on all aspects of orthopaedic surgery. It is the official journal of the Asia Pacific Orthopaedic Association. The journal welcomes and will publish materials of a diverse nature, from basic science research to clinical trials and surgical techniques. The journal encourages contributions from all parts of the world, but special emphasis is given to research of particular relevance to the Asia Pacific region.
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