Intervertebral disc degeneration (IDD) refers to the abnormal response of cell-mediated progressive structural failure. In order to understand the molecular mechanism of the maintenance and destruction of the intervertebral disc, new IDD treatment methods are developed. Here, we first analyzed the key regulators of IDD through miRNA microarrays. The cell structure and morphology were discovered by Histological and radiographic. Then, the level of miR-31-5p was disclosed by qRT-PCR. The association between miR-31-5p and SDF-1/CXCR7 axis was discovered by 3′-Untranslated region (UTR) cloning and luciferase assay. The apoptosis of cells under different treatments was disclosed by Flow cytometer. The cell proliferation was discovered by EdU assay. Finally, the protein levels of SDF-1, CXCR7, ADAMTS-5, Col II, Aggrecan and MMP13 were discovered by Western blot. The results show that miR-31-5p is a key regulator of IDD and its level is down-regulated in IDD. Overexpression of miR-31-5p facilitates NP cell proliferation, inhibits apoptosis, facilitates ECM formation and inhibits the level of matrix degrading enzymes in NP cells. The SDF-1/CXCR7 axis is the direct target of miR-31-5p. miR-31-5p acts on IDD by regulating SDF-1/CXCR7. In vitro experiments further verified that the up-regulation of miR-31-5p prevented the development of IDD. In conclusion, overexpression of miR-31-5p can inhibit IDD by regulating SDF-1/CXCR7.

中文翻译：

---

miR-31-5p在椎间盘退变发展中的作用及其治疗潜力

椎间盘退变（IDD）是指细胞介导的进行性结构衰竭的异常反应。为了了解维持和破坏椎间盘的分子机制，开发了新的IDD治疗方法。在这里，我们首先通过miRNA微阵列分析了IDD的关键调控因子。通过组织学和射线照相术发现了细胞结构和形态。然后，通过qRT-PCR公开了miR-31-5p的水平。miR-31-5p和SDF-1 / CXCR7轴之间的关联是通过3'-非翻译区（UTR）克隆和荧光素酶测定法发现的。流式细胞仪揭示了不同处理条件下细胞的凋亡情况。通过EdU测定发现细胞增殖。最后，SDF-1，CXCR7，ADAMTS-5，Col II，通过蛋白质印迹法发现了Aggrecan和MMP13。结果表明，miR-31-5p是IDD的关键调控因子，其水平在IDD中被下调。miR-31-5p的过表达促进NP细胞增殖，抑制细胞凋亡，促进ECM形成并抑制NP细胞中基质降解酶的水平。SDF-1 / CXCR7轴是miR-31-5p的直接目标。miR-31-5p通过调节SDF-1 / CXCR7对IDD起作用。体外实验进一步证实，miR-31-5p的上调阻止了IDD的发展。总之，miR-31-5p的过表达可以通过调节SDF-1 / CXCR7抑制IDD。促进ECM的形成并抑制NP细胞中基质降解酶的水平。SDF-1 / CXCR7轴是miR-31-5p的直接目标。miR-31-5p通过调节SDF-1 / CXCR7对IDD起作用。体外实验进一步证实，miR-31-5p的上调阻止了IDD的发展。总之，miR-31-5p的过表达可以通过调节SDF-1 / CXCR7抑制IDD。促进ECM的形成并抑制NP细胞中基质降解酶的水平。SDF-1 / CXCR7轴是miR-31-5p的直接目标。miR-31-5p通过调节SDF-1 / CXCR7对IDD起作用。体外实验进一步证实，miR-31-5p的上调阻止了IDD的发展。总之，miR-31-5p的过表达可以通过调节SDF-1 / CXCR7抑制IDD。