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首页> 外文期刊>Molecular medicine reports >MicroRNA-451 protects against cardiomyocyte anoxia/reoxygenation injury by inhibiting high mobility group box 1 expression
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MicroRNA-451 protects against cardiomyocyte anoxia/reoxygenation injury by inhibiting high mobility group box 1 expression

机译：MicroRNA-451通过抑制高迁移率基团box 1的表达来预防心肌细胞缺氧/复氧损伤

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摘要

High mobility group box 1 (HMGB1) protein serves an important role in myocardial ischemia/reperfusion (I/R) injury. MicroRNAs (miRNAs) are a group of small non-coding RNAs that regulate numerous signaling pathways involved in myocardial I/R injury. The present study aimed to investigate whether miR-451 protects against cardiomyocyte anoxia/reoxygenation (A/R) injury by attenuating HMGB1 expression. Neonatal rat ventricular cardiomyocytes were prepared and then subjected to A/R injury. The effect of upregulation or downregulation of miR-451 on cell viability, apoptosis, superoxide dismutase (SOD) activity, and the expression of cleaved-caspase-3 and HMGB1 were measured accordingly. A luciferase assay was performed to further confirm whether miR-451 can directly recognize the 3-untranslated region of HMGB1 in HEK293 cells. The expression of miR-451 was significantly decreased in the cardiomyocytes during A/R, and upregulation of miR-451 led to increased miR-451 expression (P<0.05). Upregulation of miR-451 significantly attenuated the loss of cardiomyocyte viability (P<0.05) and increased the intracellular levels of SOD during A/R (P<0.05). Furthermore, upregulation of miR-451 significantly decreased the apoptosis of cardiomyocytes during A/R (P<0.05). The HMGB1 mRNA and protein expression levels were significantly downregulated in the Ad-miR-451 group compared with those in the A/R group (P<0.05). In addition, upregulation of miR-451 reduced its translocation from the nucleus to the cytoplasm. The luciferase assay confirmed that HMGB1 mRNA is a direct target of miR-451 in cardiomyocytes. In conclusion, the present study suggested that upregulation of miR-451 could protect against A/R-induced cardiomyocyte injury by inhibiting HMGB1 expression.
机译：高迁移率族盒1（HMGB1）蛋白在心肌缺血/再灌注（I / R）损伤中起重要作用。微小RNA（miRNA）是一组小的非编码RNA，它们调节涉及心肌I / R损伤的众多信号通路。本研究旨在研究miR-451是否通过减弱HMGB1表达来防止心肌缺氧/复氧（A / R）损伤。制备新生大鼠心室心肌细胞，然后使其受到A / R损伤。相应地测量了miR-451上调或下调对细胞活力，凋亡，超氧化物歧化酶（SOD）活性以及裂解的caspase-3和HMGB1表达的影响。进行荧光素酶测定以进一步证实miR-451是否可以直接识别HEK293细胞中HMGB1的3-非翻译区。 A / R期间心肌细胞中miR-451的表达明显降低，miR-451的上调导致miR-451的表达增加（P <0.05）。 miR-451的上调显着减轻了心肌细胞活力的丧失（P <0.05），并增加了A / R期间细胞内SOD的水平（P <0.05）。此外，miR-451的上调显着降低了A / R期间心肌细胞的凋亡（P <0.05）。与A / R组相比，Ad-miR-451组的HMGB1 mRNA和蛋白表达水平显着下调（P <0.05）。此外，miR-451的上调减少了其从细胞核到细胞质的转运。荧光素酶测定证实，HMGB1 mRNA是心肌细胞中miR-451的直接靶标。总之，本研究表明，miR-451的上调可以通过抑制HMGB1表达来预防A / R诱导的心肌细胞损伤。

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