| 崔冰,柴巧英,李鑫平,王丹丹,陈兰兰,韩继如,张海军.circ_0068655通过吸附miR-498促进心肌细胞HCM凋亡.[J].中南医学科学杂志.,2024,(4):539-543, 573. |
| circ_0068655通过吸附miR-498促进心肌细胞HCM凋亡 |
| circ_0068655 can promote apoptosis of cardiomyocyte HCM by sponging miR-498 |
| 投稿时间：2023-08-09 修订日期：2024-12-27 |
| DOI：10.15972/j.cnki.43-1509/r.2024.04.008 |
| 中文关键词: 心肌细胞 凋亡 circ_0068655 miR-498 |
| 英文关键词:cardiomyocytes apoptosis circ_0068655 miR-498 |
| 基金项目:河北省医学科学研究课题(20220012；20200438) |
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| 中文摘要: |
| 目的探讨环状RNA(circRNA)_0068655对心肌细胞HCM凋亡的影响。 方法12只雄性大鼠随机分为假手术组(Sham组)和心肌梗死组(MI组),qRT-PCR检测两组心肌组织中circ_0068655和miR-498表达水平,Western blotting检测两组心肌组织中凋亡相关蛋白的表达。将HCM分为空白对照组、circ_0068655敲低组(sh-circ_0068655组),circ_0068655过表达组、低氧刺激组(Hypoxia组)、敲低对照+低氧刺激组(sh-ctrl+hypoxia组)、circ_0068655敲低+低氧刺激组(sh-circ_0068655+hypoxia组),缺氧的HCM分为敲低对照+miR-498-inhibitor-NC组(sh-ctrl+miR-498-inhibitor-NC组)、circ_0068655敲低+miR-498-inhibitor-NC组(sh-circ_0068655+miR-498-inhibitor-NC组)及circ_0068655敲低+miR-498-inhibitor组(sh-circ_0068655+miR-498-inhibitor组),qRT-PCR检测各组HCM中circ_0068655和miR-498表达量,CCK-8、ELISA及Transwell检测细胞活性、凋亡、迁移及侵袭能力。RNA pull-down及双荧光素酶实验分析circ_0068655和miR-498结合关系。 结果MI大鼠心肌组织中circ_0068655的表达高于Sham组,miR-498表达低于Sham组,敲低circ_0068655可以改善缺氧诱导的HCM心肌细胞活力,提高心肌细胞迁移及侵袭能力,降低细胞凋亡率及凋亡相关蛋白表达。circ_0068655可结合并负向调节miR-498的表达。miR-498抑制剂可抑制敲低circ_0068655对缺氧心肌细胞保护作用。 结论circ_0068655能通过吸附miR-498促进心肌梗死及心肌细胞凋亡。 |
| 英文摘要: |
| AimTo investigate the effects of circular _0068655 on the apoptosis of cardiomyocytes. MethodsTwelve male rats were randomly divided into Sham group and acute myocardial infarction group (MI group). qRT-PCR was used to detect the expression of circ_0068655 and miR-498, and Western blotting was performed to detect the expression of apoptosis-related proteins in myocardium of two groups of rats. HCM were divided into blank control group, circ_0068655 knockdown group (sh-circ_0068655 group), circ_0068655 overexpression group, hypoxia group (hypoxia group), knockdown control+hypoxia group (sh-ctrl+hypoxia group), circ_0068655 knockdown+hypoxia (sh-circ_0068655+hypoxia group). Hypoxic HCM were divided into knockdown control+miR-498-inhibitor-NC group (sh-ctrl+miR-498-inhibitor-NC group), circ_0068655 knockdown+miR-498-inhibitor-NC group (sh-circ _ 0068655+miR-498-inhibitor-NCgroup) and circ _ 0068655 knockdown+miR-498-inhibitor group (sh-circ_0068655+miR-498-inhibitor group). The expression levels of circ_0068655 and miR-498 in HCM were detected by qRT-PCR, and cell activity, apoptosis, migration and invasion were detected by CCK-8, ELISA and Transwell methods in all groups. The binding relationship between circ_0068655 and miR-498 was analyzed by RNA pull-down and dual luciferase assays. ResultsThe expression of circ_0068655 in myocardial tissue of MI rats was higher than that of Sham group, and the expression of miR-498 was lower than that of Sham group.Knockdown of circ_0068655 could improve the viability of HCM cardiomyocytes induced by hypoxia, improve the migration and invasion ability of cardiomyocytes, and reduce the apoptosis rate and apoptosis-related protein expression. circ_0068655 can bind and negatively regulate the expression of miR-498. miR-498-inhibitors can inhibit the protective effects of circ_0068655 knockdown on hypoxic cardiomyocytes. Conclusioncirc_0068655 can promote the apoptosis of cardiomyocytes in myocardial infarction by sponging miR-498. |
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