The sensitivity of myocardium is enhanced to ischemia/reperfusion (I/R) injury under PM2.5 exposure. It is still under prelude for lncRNA-miRNA pair in the study of aggravated myocardial I/R injury under PM2.5 exposure. In this study, we first built a rat model of 30 min ischemia and 24 h reperfusion followed PM2.5 (6.0 mg/kg) exposure. We found PM2.5 exposure could obviously aggravate I/R injury in the fields of myocardium damage, apoptosis levels and cardiac function which were evaluated by TTC staining, TUNEL and echocardiography, respectively. Then, based on results of sequencing and RT-qPCR, we selected NONRATT003473.2 in the follow-up experiments and named this lncRNA as PM2.5 exposure aggravated myocardial I/R injury lncRNA (PEAMIR). Consistent with the results rat model, we confirmed PEAMIR to be a protective lncRNA against PM + HR triggered damages in H9c2 cells. Next, according to the bioinformatics analysis from miRanda database and a series of gain- and loss-of-function experiments, we proved PEAMIR to be a ceRNA for miR-29b-3p to inhibit cardiac inflammation and apoptosis. Finally, using Target-Scan database, the conserved binding sites for miR-29b-3p was identified in the 3'UTR of PI3K (p85a), a key protein of apoptosis. Our subsequent experiments validated the regulatory relationship between PEAMIR-miR-29b-3p ceRNA pair and PI3K (p85a)/Akt/GSK3b/p53 cascade pathway. In conclusion, our study demonstrated the role and mechanism of PEAMIR in the augment of I/R injury under PM2.5 exposure, suggesting a promising strategy for the prevention and treatment of I/R injury under PM2.5 exposure.

中文翻译：

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LncRNA PEAMIR作为miR-29b-3p的竞争内源性RNA，在PM2.5暴露加剧的心肌缺血/再灌注损伤中抑制细胞凋亡和炎症反应。

在PM2.5暴露下，心肌对缺血/再灌注（I / R）损伤的敏感性增强。在PM2.5暴露下加重心肌I / R损伤的研究中，lncRNA-miRNA对仍处于序幕。在这项研究中，我们首先建立了30分钟缺血和24小时再灌注后再暴露PM2.5（6.0 mg / kg）的大鼠模型。我们发现，分别通过TTC染色，TUNEL和超声心动图评估，暴露于PM2.5会明显加重心肌损伤，细胞凋亡水平和心功能领域的I / R损伤。然后，基于测序和RT-qPCR的结果，我们在后续实验中选择了NONRATT003473.2，并将该lncRNA命名为PM2.5暴露加重了心肌I / R损伤lncRNA（PEAMIR）。与结果大鼠模型一致，我们证实PEAMIR是针对PM + HR触发的H9c2细胞损伤的保护性lncRNA。接下来，根据来自miRanda数据库的生物信息学分析以及一系列功能获得和丧失的实验，我们证明了PEAMIR是miR-29b-3p抑制心脏炎症和细胞凋亡的ceRNA。最后，使用Target-Scan数据库，在凋亡的关键蛋白PI3K（p85a）的3'UTR中鉴定了miR-29b-3p的保守结合位点。我们随后的实验验证了PEAMIR-miR-29b-3p ceRNA对与PI3K（p85a）/ Akt / GSK3b / p53级联途径之间的调控关系。总之，我们的研究证明了PEAMIR在PM2.5暴露下增加I / R损伤中的作用和机制，为预防和治疗PM2.5暴露下的I / R损伤提供了有希望的策略。