a Department of Vascular Surgery, Jining No.1 People's Hospital , Jining , China.
b Affiliated Jining No.1 People's Hospital of Jining Medical University, Jining Medical University , Jining , China.
Artif Cells Nanomed Biotechnol. 2019 Dec;47(1):2698-2705. doi: 10.1080/21691401.2019.1634577.
H19 is the first identified long non-coding RNA (lncRNA) whose function in diverse cancers and non-cancerous disease states has been widely studied. The objective of this study was to study the functional role of H19 in vascular endothelial cells. We found that H19 overexpression significantly increased HMEC-1 cells viability, migration and tube-formation capacity. Meanwhile, H19 overexpression up-regulated the protein levels of MMP-2, MMP-9, VEGF and eNOS, and down-regulated RNA level of miR-181a. These alterations, induced by H19 overexpression were abolished by miR-181a overexpression, while they were enhanced when miR-181a was silenced. And also, overexpression of H19 activated JNK and AMPK signalling, which could be eliminated by miR-181a overexpression and accelerated by miR-181a suppression. In conclusion, overexpression of H19 improved HMEC-1 cells viability, migration and tube-formation capacity. H19 exerted pro-angiogenic effects possibly by down-regulating miR-181a, and thus activating JNK and AMPK signalling pathways.
H19 是第一个被鉴定的长链非编码 RNA（lncRNA），其在多种癌症和非癌症疾病状态下的功能已被广泛研究。本研究的目的是研究 H19 在血管内皮细胞中的功能作用。我们发现 H19 的过表达显著增加了 HMEC-1 细胞的活力、迁移和管状形成能力。同时，H19 的过表达上调了 MMP-2、MMP-9、VEGF 和 eNOS 的蛋白水平，下调了 miR-181a 的 RNA 水平。这些由 H19 过表达引起的变化，被 miR-181a 的过表达所消除，而当 miR-181a 被沉默时则增强。此外，H19 的过表达激活了 JNK 和 AMPK 信号通路，而 miR-181a 的过表达可以消除这种激活，而 miR-181a 的抑制则加速了这种激活。总之，H19 的过表达提高了 HMEC-1 细胞的活力、迁移和管状形成能力。H19 通过下调 miR-181a 发挥促血管生成作用，从而激活 JNK 和 AMPK 信号通路。
