Department of Vascular Surgery, Jining No. 1 People's Hospital, Jining, Shandong, China.
Affiliated Jining No. 1 People's Hospital of Jining Medical University, Jining Medical University, Jining, Shandong, China.
J Biochem Mol Toxicol. 2020 May;34(5):e22468. doi: 10.1002/jbt.22468. Epub 2020 Feb 13.
Atherosclerosis is one of the most common and crucial heart diseases involving the heart and brain. At present, atherosclerosis and its major complications comprise the leading causes of death worldwide. Our purpose was to identify the role of ciRS-7 in atherosclerosis. Tubulogenesis of HMEC-1 cell was evaluated utilizing tube formation assay. Cell Counting Kit-8 assay and flow cytometry were utilized to test viability and apoptosis. Migration assay was utilized to determine the migration capacity of experimental cells. Western blot was applied to examine apoptosis and tube formation-associated protein expression. In addition, the above experiments were repeated when silencing ciRS-7, overexpressing ciRS-7, and upregulating miR-26a-5p. HMEC-1 cells formed tube-like structures over time. Silencing ciRS-7 suppressed viability, migration, and tube formation but promoted apoptosis. Oppositely, overexpressing ciRS-7 reversed the effect in HMEC-1 cells. miR-26a-5p expression was elevated by silencing ciRS-7 and reduced by overexpressing ciRS-7. Moreover, overexpressing ciRS-7 facilitated viability, migration, and tube formation via upregulating miR-26a-5p. Conclusively, overexpressing ciRS-7 mobilized phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) pathway and suppressed c-Jun N-terminal kinase (JNK)/p38 pathway. ciRS-7 exerted influence on apoptosis, viability, migration, and tube formation through mediating PI3K/AKT and JNK/p38 pathways by miR-26a-5p downregulation in HMEC-1 cells.
动脉粥样硬化是最常见和最重要的涉及心脏和大脑的心脏病之一。目前，动脉粥样硬化及其主要并发症构成了全球范围内的主要死亡原因。我们的目的是确定 ciRS-7 在动脉粥样硬化中的作用。利用管形成测定法评估 HMEC-1 细胞的管状形成。使用细胞计数试剂盒-8 测定法和流式细胞术测试细胞活力和凋亡。迁移测定法用于确定实验细胞的迁移能力。Western blot 用于检查凋亡和管形成相关蛋白的表达。此外，当沉默 ciRS-7、过表达 ciRS-7 和上调 miR-26a-5p 时，重复了上述实验。HMEC-1 细胞随着时间的推移形成管状结构。沉默 ciRS-7 抑制了活力、迁移和管状形成，但促进了凋亡。相反，过表达 ciRS-7 逆转了 HMEC-1 细胞中的作用。沉默 ciRS-7 可上调 miR-26a-5p 表达，而过表达 ciRS-7 则降低了 miR-26a-5p 的表达。此外，过表达 ciRS-7 通过上调 miR-26a-5p 促进了活力、迁移和管状形成。总之，过表达 ciRS-7 激活了磷脂酰肌醇 3-激酶/蛋白激酶 B（PI3K/AKT）途径，并抑制了 c-Jun N-末端激酶（JNK）/p38 途径。ciRS-7 通过下调 miR-26a-5p 对 HMEC-1 细胞中的 PI3K/AKT 和 JNK/p38 途径产生影响，从而对凋亡、活力、迁移和管状形成产生影响。
