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Downregulation of miR-483-5p decreases hypoxia-induced injury in human cardiomyocytes by targeting MAPK3.
Cellular & Molecular Biology Letters ( IF 9.2 ) Pub Date : 2020-03-17 , DOI: 10.1186/s11658-020-00213-0
Yan Hao 1 , Haitao Yuan 1 , Houzhi Yu 1
Affiliation  

MiR-483-5p was recently identified as a risk factor in the early stages of acute myocardial infarction (AMI) patients. Here, we further investigated how miR-483-5p affects cardiomyocyte apoptosis and oxidative stress under hypoxic conditions. Plasma samples were collected from AMI patients and healthy volunteers. The expression of miR-483-5p was determined using quantitative real-time PCR. An in vitro hypoxic model was constructed to mimic AMI in AC16 cells. Cell viability, apoptosis and oxidative stress biomarker levels (MDA, SOD and CAT) were respectively determined using CCK-8, flow cytometry and commercial assay kits. The expression levels of miR-483-5p were significantly higher in AMI patients than in control subjects. Circulating levels of miR-483-5p positively correlated with creatine kinase MB isoform (CK-MB) and cardiac troponin I (cTnI) levels. The in vitro experiments showed that the expression levels of miR-483-5p were also upregulated in hypoxia-induced AC16 cell injury. MiR-483-5p overexpression significantly increased hypoxia-induced cardiomyocyte apoptosis and oxidative stress, while knockdown attenuated these effects. Mechanistically, miR-483-5p directly targets MAPK3 in AC16 cells. Furthermore, the protective effects of miR-483-5p knockdown against hypoxia-induced cardiomyocyte injury are partially dependent on MAPK3. MiR-483-5p, which targets MAPK3, might be a potential therapeutic target for the diagnosis and prevention of hypoxia-induced myocardial injury.

中文翻译:

miR-483-5p 的下调通过靶向 MAPK3 减少缺氧诱导的人心肌细胞损伤。

MiR-483-5p 最近被确定为急性心肌梗死 (AMI) 患者早期阶段的危险因素。在这里,我们进一步研究了 miR-483-5p 如何在缺氧条件下影响心肌细胞凋亡和氧化应激。血浆样本采集自 AMI 患者和健康志愿者。使用定量实时PCR测定miR-483-5p的表达。构建体外缺氧模型以模拟 AC16 细胞中的 AMI。使用 CCK-8、流式细胞术和商业化验试剂盒分别测定细胞活力、细胞凋亡和氧化应激生物标志物水平(MDA、SOD 和 CAT)。AMI患者中miR-483-5p的表达水平显着高于对照组。循环中的 miR-483-5p 水平与肌酸激酶 MB 亚型 (CK-MB) 和心肌肌钙蛋白 I (cTnI) 水平呈正相关。体外实验表明,在缺氧诱导的 AC16 细胞损伤中,miR-483-5p 的表达水平也上调。MiR-483-5p 过表达显着增加了缺氧诱导的心肌细胞凋亡和氧化应激,而敲低则减弱了这些影响。机制上,miR-483-5p 直接靶向 AC16 细胞中的 MAPK3。此外,miR-483-5p 敲低对缺氧诱导的心肌细胞损伤的保护作用部分依赖于 MAPK3。靶向 MAPK3 的 MiR-483-5p 可能是诊断和预防缺氧性心肌损伤的潜在治疗靶点。体外实验表明,在缺氧诱导的 AC16 细胞损伤中,miR-483-5p 的表达水平也上调。MiR-483-5p 过表达显着增加了缺氧诱导的心肌细胞凋亡和氧化应激,而敲低则减弱了这些影响。机制上,miR-483-5p 直接靶向 AC16 细胞中的 MAPK3。此外,miR-483-5p 敲低对缺氧诱导的心肌细胞损伤的保护作用部分依赖于 MAPK3。靶向 MAPK3 的 MiR-483-5p 可能是诊断和预防缺氧性心肌损伤的潜在治疗靶点。体外实验表明,在缺氧诱导的 AC16 细胞损伤中,miR-483-5p 的表达水平也上调。MiR-483-5p 过表达显着增加了缺氧诱导的心肌细胞凋亡和氧化应激,而敲低则减弱了这些影响。机制上,miR-483-5p 直接靶向 AC16 细胞中的 MAPK3。此外,miR-483-5p 敲低对缺氧诱导的心肌细胞损伤的保护作用部分依赖于 MAPK3。靶向 MAPK3 的 MiR-483-5p 可能是诊断和预防缺氧性心肌损伤的潜在治疗靶点。miR-483-5p 直接靶向 AC16 细胞中的 MAPK3。此外,miR-483-5p 敲低对缺氧诱导的心肌细胞损伤的保护作用部分依赖于 MAPK3。靶向 MAPK3 的 MiR-483-5p 可能是诊断和预防缺氧性心肌损伤的潜在治疗靶点。miR-483-5p 直接靶向 AC16 细胞中的 MAPK3。此外,miR-483-5p 敲低对缺氧诱导的心肌细胞损伤的保护作用部分依赖于 MAPK3。靶向 MAPK3 的 MiR-483-5p 可能是诊断和预防缺氧性心肌损伤的潜在治疗靶点。
更新日期:2020-03-17
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