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首页> 外文期刊>Cellular Physiology and Biochemistry >Exosomes from MiR-126-Overexpressing Adscs Are Therapeutic in Relieving Acute Myocardial Ischaemic Injury
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Exosomes from MiR-126-Overexpressing Adscs Are Therapeutic in Relieving Acute Myocardial Ischaemic Injury

机译:MiR-126过表达的Adscs的外泌体在缓解急性心肌缺血性损伤中具有治疗作用

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biBackground/Aims/i/b Recent studies have indicated that exosomes play an important role in adipose-derived stem cell (ADSC) transplant-mediated ischaemic heart disease therapy. However, the treatment effect is not obvious. The aim of this study is to investigate whether ADSC-derived exosomes enriched with microRNA (miR)-126 have a more protective effect on acute myocardial infarction (AMI). biMethods/i/b Exosomes were characterized by transmission electron microscopy, and the exosome particles were further examined using nanoparticle tracking analyses. A rat model of myocardial infarction and iin vitro/i model of hypoxia-induced H9c2 myocardial cell injury were established to study the protective mechanism of exosomes from miR-126-overexpressing ADSCs. biResults/i/b The iin vitro/i results showed that exosomes derived from miR-126-overexpressing ADSCs decreased H9c2 myocardial cell injury by reducing inflammation factor expression during hypoxia induction. The miR-126-enriched exosomes also decreased the expression of fibrosis-related proteins of H9c2 cells under hypoxic conditions. Matrigel® and Transwell® assays showed that miR-126-enriched exosomes significantly promoted microvascular generation and migration, respectively. iIn vivo/i studies confirmed that exosomes derived from ADSCs significantly decreased the myocardial injury area of infarction, especially after miR-126-enriched exosome treatment. Cardiac fibrosis and inflammatory cytokine expression were also decreased after treatment with miR-126-enriched exosomes. However, blood vessel formation was promoted in the infarction region of AMI rats. biConclusions/i/b The results suggested that the expression of miR-126-enhanced ADSC-derived exosomes prevented myocardial damage by protecting myocardial cells from apoptosis, inflammation, fibrosis, and increased angiogenesis.
机译:背景/目标 最近的研究表明,外泌体在脂肪干细胞(ADSC)移植介导的缺血性心脏病治疗中起着重要作用。但是,治疗效果不明显。这项研究的目的是调查富含microRNA(miR)-126的ADSC衍生的外泌体是否对急性心肌梗死(AMI)具有更好的保护作用。 方法 利用透射电子显微镜对外泌体进行了表征,并使用纳米粒子跟踪分析进一步检查了外泌体颗粒。建立大鼠心肌梗死模型和低氧诱导的H9c2心肌细胞损伤的体外模型,以研究miR-126过表达的ADSCs的外来体保护机制。 结果 体外结果表明,miR-126过表达的ADSC的外泌体通过减少低氧诱导过程中的炎症因子表达来降低H9c2心肌细胞损伤。在低氧条件下,富含miR-126的外泌体也降低了H9c2细胞纤维化相关蛋白的表达。 Matrigel®和Transwell®分析表明,富含miR-126的外泌体显着促进了微血管的生成和迁移。 体内研究证实,源自ADSC的外泌体显着减少了梗塞的心肌损伤区域,尤其是在富含miR-126的外泌体治疗后。富含miR-126的外泌体治疗后,心脏纤维化和炎性细胞因子的表达也降低了。然而,在AMI大鼠的梗塞区域中促进了血管形成。 结论 结果表明,miR-126增强的ADSC衍生的外泌体的表达通过保护心肌细胞免于凋亡,炎症,纤维化和增加的血管生成而阻止了心肌损伤。

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