MicroRNA-21 mediates the protective role of emulsified isoflurane against myocardial ischemia/reperfusion injury in mice by targeting SPP1 |
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| Institution: | 1. Cancer Research Program, Julius L. Chambers Biomedical Biotechnology Research Institute, North Carolina Central University, 700 George Street, Durham, NC 27707, USA;2. Bioinformatics Research Center, North Carolina State University, Raleigh, NC 27607, USA;3. Euclados Bioinformatics Solutions, Cary, NC 27519, USA;4. Center for Gastrointestinal Biology and Disease, Division of Gastroenterology and Hepatology, Department of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA;1. Department of Biochemistry, University of Kashmir, Srinagar 190006, India;2. Department of Biotechnology, University of Kashmir, Srinagar 190006, India |
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| Abstract: | Isoflurane has demonstrated to exert protective impacts against ischemia/reperfusion (I/R) injury in some organs. This research explored the role of emulsified isoflurane (EI) in myocardial I/R injury through the interaction with microRNA-21 (miR-21). The myocardial I/R injury mouse models established by coronary artery ligation were respectively treated with EI, miR-21 mimic/inhibitor or silenced secreted phosphoprotein 1 (SPP1) plasmids. Then, the pathology, fibrosis and cardiomyocyte apoptosis in mouse myocardial tissues were observed. Furthermore, the expression levels of miR-21, SPP1, oxidative stress indices, inflammatory factors and apoptotic proteins in mouse myocardial tissues were determined. The targeting relation between miR-21 and SPP1 was confirmed. MiR-21 was poorly expressed and SPP1 was highly expressed in myocardial I/R injury mice. EI treatment, elevated miR-21, or silenced SPP1 improved cardiac function and suppressed the oxidative stress, myocardial fibrosis, inflammatory reaction and cardiomyocyte apoptosis in myocardial I/R injury mice, thereby reliving the myocardial I/R injury. These therapeutic effects of EI were repressed by miR-21 inhibition. Additionally, SPP1 was targeted by miR-21. Results in our research indicated that miR-21 mediated the therapeutic effect of EI on myocardial I/R injury in mice by targeting SPP1. This study may provide a novel treatment strategy for myocardial I/R injury. |
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