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首页> 外文期刊>Cellular Physiology and Biochemistry >MiR-1246 Promotes LPS-Induced Inflammatory Injury in Chondrogenic Cells ATDC5 by Targeting HNF4?3
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MiR-1246 Promotes LPS-Induced Inflammatory Injury in Chondrogenic Cells ATDC5 by Targeting HNF4?3

机译：MiR-1246通过靶向HNF4？3促进软骨细胞ATDC5中LPS诱导的炎性损伤。

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>Background/Aims: Osteoarthritis (OA) is a common inflammatory joint disease. miRNAs are associated with OA and functionally implicated in the pathogenesis of the disease. In the present study, we investigated the role of miR-1246 in the lipopolysaccharide (LPS)-induced inflammatory injury of ATDC5 cells. Methods: ATDC5 cells were cultured and treated with LPS in a series of concentration (0, 1, 5, and 10 ?μg/ml) for 5 h. The cells were transfected with miR-1246-mimic, inhibitor, si-HNF4?3 or negative control, then were assessed for cell viability using CCK8 assay, apoptosis by flow-cytometry and expressions of miR-1246 and pro-inflammatory cytokines by qRT-PCR and western blot analysis. Results: Cell viability was significantly reduced and cell apoptosis was added in ATDC5 cells injured with LPS at the dosage of 5 and 10 ?μg/ml. Relative mRNA expressions of pro-inflammatory cytokines (IL-1?2, IL-6, IL-8 and TNF-?±) were significantly increased. miR-1246 was up-regulated in ATDC5 cells treated with LPS. Moreover, miR-1246 overexpression aggravated LPS-induced decrease in cell viability, increase in apoptosis and overproduction of pro-inflammatory factors. mRNA and protein expressions of HNF4?3 were significantly suppressed in cells transfected with miR-124-mimic. Further, miR-1246 knockdown alleviated LPS-induced inflammatory injury by up-regulating the expression of HNF4?3 and activation of PI3K/AKT and JAK/STAT pathways. Conclusions: Suppression of miR-1246 alleviated LPS-induced inflammatory injury in chondrogenic ADTC5 cells by up-regulation of HNF4?3 and activation of PI3K/AKT and JAK/STAT pathways. The findings of this study will provide a novel viewpoint regarding miR-1246 target for clinical.
机译：> 背景/目的： 骨关节炎（OA）是一种常见的炎症性关节疾病。 miRNA与OA相关，并且在功能上与疾病的发病机制有关。在本研究中，我们调查了miR-1246在脂多糖（LPS）诱导的ATDC5细胞炎症性损伤中的作用。 方法： 培养ATDC5细胞，并用一系列浓度（0、1、5和10μg/ ml）的LPS处理5 h。用miR-1246-mimic，抑制剂，si-HNF4？3或阴性对照转染细胞，然后使用CCK8分析评估细胞活力，通过流式细胞术评估细胞凋亡，并通过qRT评估miR-1246和促炎细胞因子的表达。 -PCR和蛋白质印迹分析。 结果： 以5和10μg/ ml的剂量，LPS损伤的ATDC5细胞的细胞活力显着降低，并增加了细胞凋亡。促炎细胞因子（IL-1？2，IL-6，IL-8和TNF-？±）的相对mRNA表达显着增加。在用LPS处理的ATDC5细胞中，miR-1246上调。而且，miR-1246的过表达加剧了LPS诱导的细胞活力下降，细胞凋亡增加和促炎因子的过度产生。在用miR-124-mimic转染的细胞中，HNF4β3的mRNA和蛋白表达被显着抑制。此外，miR-1246的敲低可以通过上调HNF4α3的表达以及PI3K / AKT和JAK / STAT通路的激活来减轻LPS引起的炎症损伤。 结论： 抑制miR-1246可通过上调HNF4？3以及激活PI3K / AKT和JAK / STAT途径减轻脂多糖诱导的软骨ADDC5细胞的炎性损伤。 。这项研究的发现将为miR-1246靶标提供新的观点。

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