Sun Jia, Chen Jintao, Cao Juan, Li Tianxiang, Zhuang Shaoxia, Jiang Xiufeng
Wuxi People's Hospital Affiliated to Nanjing Medical University, Wuxi 214023, Jiangsu, China.
Oncotarget. 2016 Sep 13;7(37):59429-59440. doi: 10.18632/oncotarget.10683.
Considerable attentions have been focused on the treatment of lung injury using mesenchymal stem cells that can replenish damaged tissues including the blood vessels. In human lung-derived mesenchymal stem cells (hL-MSC), we investigated the potential role of an IL-1β-stimulated miR-433 pathway in angiogenesis in vitro. The expressions of miR-433 and its target genes were examined in cells treated with IL-1β. The angiogenic activity of hL-MSC was studied by cell migration and tube formation assays in which miR-433 levels were manipulated. The reporter assay and chromatin immunoprecipitation (ChIP) were also performed to analyze the underlying regulations. We found that the expression of miR-433 was enhanced in hL-MSC by IL-1β in a NF-κB dependent manner via a NF-κB binding site at its promoter region. The effects of IL-1β on promoting angiogenic activities in hL-MSC can be mimicked by the overexpression of miR-433 and were blocked by anti-miR-433. Mechanistically, our data suggested that miR-433 directly targets the 3'-UTR of Dickkopf Wnt signaling pathway inhibitor 1 (DKK1) mRNA and decreases its expression. Consistently, the expression of β-catenin, the major mediator of canonical Wnt pathway that is capable of inducing endothelial differentiation and angiogenesis, was upregulated by IL-1β through miR-433. Thus, increasing miR-433 expression by IL-1β in mesenchymal stem cells could stimulate their capacity of vascular remodeling for efficient repair processes, which may be utilized as a therapeutic target in patients suffering from severe lung injury.
相当多的注意力都集中在使用间充质干细胞治疗肺损伤上,间充质干细胞可以补充包括血管在内的受损组织。在人肺源性间充质干细胞(hL-MSC)中,我们研究了白细胞介素-1β(IL-1β)刺激的miR-433通路在体外血管生成中的潜在作用。在用IL-1β处理的细胞中检测了miR-433及其靶基因的表达。通过细胞迁移和管形成实验研究了hL-MSC的血管生成活性,其中对miR-433水平进行了调控。还进行了报告基因实验和染色质免疫沉淀(ChIP)分析潜在的调控机制。我们发现,IL-1β通过其启动子区域的核因子κB(NF-κB)结合位点以NF-κB依赖的方式增强了hL-MSC中miR-433的表达。miR-433的过表达可模拟IL-1β对hL-MSC血管生成活性的促进作用,而抗miR-433则可阻断这种作用。从机制上讲,我们的数据表明,miR-433直接靶向Dickkopf Wnt信号通路抑制剂1(DKK1)mRNA的3'-非翻译区(3'-UTR)并降低其表达。同样,作为经典Wnt通路的主要介导因子、能够诱导内皮细胞分化和血管生成的β-连环蛋白(β-catenin)的表达通过miR-433被IL-1β上调。因此,IL-1β在间充质干细胞中增加miR-433的表达可以刺激它们进行血管重塑以实现高效修复过程的能力,这可能被用作严重肺损伤患者的治疗靶点。