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首页> 外文期刊>Acta biomaterialia >Injectable hyaluronic acid down-regulates interferon signaling molecules, IGFBP3 and IFIT3 in the bovine intervertebral disc
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Injectable hyaluronic acid down-regulates interferon signaling molecules, IGFBP3 and IFIT3 in the bovine intervertebral disc

机译：可注射透明质酸下调干扰素信号分子，IgFBP3和IFIT3在牛椎间盘中

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Low back pain which is a major cause of disability for people aged between 20 and 50 years imposes a serious socio-economic burden. The current focus of regenerative medicine is on identifying molecular markers to facilitate the design of targeted therapeutics. Previously, we have demonstrated that expression of the anti-proliferative interferon-induced protein with tetratricopeptide repeats 3 (IFIT3) and proapoptotic insulin-like growth factor-binding protein-3 (IGFBP3), are up-regulated as downstream targets of the inflammatory cytokine interferon alpha (IFN alpha) signaling pathway in the human annulus fibrosus (AF). Here, we hypothesised that injection of hyaluronic acid (HA) would have an anti-inflammatory and matrix modulatory effect on injured and IFN alpha(2)beta inflamed bovine intervertebral discs (IVD). Discs with an AF defect and challenged with IFN alpha(2)beta were used in a bovine IVD organ culture model to test the effect of HA on the IFN alpha(2)beta pathway, as well as the matrix proteins aggrecan and collagen I. qRT-PCR was used to assess the gene expression of IFN alpha(2)beta signaling molecules. Additionally, immunostaining was used to measure protein expression. Our results show that HA treatment significantly down-regulates IFNARI, IFNAR2, STAT1/2, JAK1, IFIT3 and IGFBP3 mRNA expression in the inflamed groups. Protein analysis confirmed the PCR results. In the extracellular matrix, aggrecan and collagen I were up-regulated while ADAMTS4 was down-regulated upon treatment of the injured and inflamed discs with HA. Hence, HA demonstrates both an anti-inflammatory role, resulting in the down-regulation of IFIT3 and IGFBP3 in the AF, and a matrix modulatory effect by up-regulating aggrecan and collagen I expression.
机译：低腰疼痛是20至50岁之间的残疾的主要原因强加了严重的社会经济负担。再生药物的目前的重点是鉴定分子标记，以促进靶向治疗的设计。以前，我们已经证明，抗增殖干扰素诱导的蛋白质与四氢肽的表达重复3（IFIT3）和促凋亡的胰岛素样生长因子结合蛋白-3（IgFBP3），被上调为炎症细胞因子的下游靶标人体环纤维（AF）中的干扰素α（IFNα）信号传导途径。在这里，我们假设注射透明质酸（HA）将对受伤和IFNα（2）β发炎牛椎间盘（IVD）的IFNα（2）β进行抗炎和基质调节作用。具有AF缺陷和用IFNα（2）β受到挑战的磁盘在牛IVD器官培养模型中用于测试HA对IFNα（2）β途径的影响，以及基质蛋白质蛋白和胶原蛋白I. QRT-PCR用于评估IFNα（2）β信号分子的基因表达。另外，使用免疫染色来测量蛋白质表达。我们的研究结果表明，HA治疗明显下调Ifnari，IFNAR2，Stat1 / 2，JAK1，IFIT3和IGFBP3 mRNA表达在发芽的群体中。蛋白质分析证实了PCR结果。在细胞外基质中，骨髓和胶原蛋白I上调，而Adamts4在用HA处理受伤和发炎的椎间盘时被下调。因此，HA证明了抗炎症作用，导致AFIT3和IGFBP3的下调，通过Up-Crommating Excrececan和胶原蛋白表达的基质调节效果。

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