1. miR-652-3p Suppressed the Protective Effects of Isoflurane Against Myocardial Injury in Hypoxia/Reoxygenation by Targeting ISL1.
- Author
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Qi K, Cao F, Wang J, Wang Y, and Li G
- Subjects
- Animals, Cell Line, Rats, Signal Transduction drug effects, Tumor Necrosis Factor-alpha metabolism, Gene Expression Regulation drug effects, Inflammation Mediators metabolism, Creatine Kinase, MB Form metabolism, Creatine Kinase, MB Form blood, Troponin I metabolism, Cytoprotection, MicroRNAs metabolism, MicroRNAs genetics, Isoflurane pharmacology, LIM-Homeodomain Proteins metabolism, LIM-Homeodomain Proteins genetics, Myocytes, Cardiac drug effects, Myocytes, Cardiac pathology, Myocytes, Cardiac metabolism, Myocytes, Cardiac enzymology, Myocardial Reperfusion Injury pathology, Myocardial Reperfusion Injury prevention & control, Myocardial Reperfusion Injury metabolism, Myocardial Reperfusion Injury genetics, Apoptosis drug effects, Cell Hypoxia, Transcription Factors metabolism, Transcription Factors genetics, Interleukin-6 metabolism, Interleukin-6 genetics
- Abstract
This research is concentrated on investigating the role and mechanism of miR-652-3p in the protective effects of isoflurane (ISO) against myocardial ischemia-reperfusion (I/R) injury. H9c2 cells underwent pretreatment with varying concentrations of ISO, and subsequently, a hypoxia/reoxygenation (H/R) model was constructed. The levels of miR-652-3p, ISL LIM homeobox 1 (ISL1), and inflammatory cytokines interleukin (IL)-6 and tumor necrosis factor-alpha (TNF-α) were evaluated through reverse transcription polymerase chain reaction (RT-qPCR). Enzyme-linked immunosorbent assay was employed to investigate concentrations of myocardial injury markers, such as creatine kinase-MB (CK-MB) and cardiac troponin I (cTnI). Cell counting kit-8 was used to evaluate cell viability, while flow cytometry was utilized to measure apoptosis. Additionally, a dual luciferase reporter assay was conducted to validate the targeting relationship between ISL1 and miR-652-3p. Herein, we confirmed that the level of miR-652-3p was gradually increased with prolonged hypoxia; nevertheless, this increase was suppressed by ISO pretreatment (P < 0.05). Additionally, ISO pretreatment prevented the decrease in cell viability, increase in apoptosis, and overproduction of IL-6, TNF-α, CK-MB, and cTnI induced by H/R (P < 0.05). However, the inhibitory effects of ISO were counteracted by the increased levels of miR-652-3p (P < 0.05). ISL1 is a potential target of miR-652-3p. H/R induction suppressed ISL1 levels compared to the control, but ISO treatment increased its expression (P < 0.05). Overexpression of ISL1 inhibited the elimination of the protective effect of ISO on myocardial damage induced by the elevation of miR-652-3p (P < 0.05). The findings of this research confirm that miR-652-3p attenuated the protective effect of ISO on cardiomyocytes in myocardial ischemia by targeting ISL1., (© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)
- Published
- 2024
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