LncRNA AC005332.7 Inhibited Ferroptosis to Alleviate Acute Myocardial Infarction Through Regulating miR-331-3p/CCND2 Axis

Rixin Dai; Xiheng Yang; Wujin He; Qiang Su; Xuexin Deng; Juanfen Li

doi:https://doi.org/10.4070/kcj.2022.0242

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자료유형: 학술저널

저자정보: Rixin Dai (The Affiliated Hospital of Guilin Medical University) Xiheng Yang (The Affiliated Hospital of Guilin Medical University) Wujin He (The Affiliated Hospital of Guilin Medical University) Qiang Su (The Affiliated Hospital of Guilin Medical University) Xuexin Deng (The Affiliated Hospital of Guilin Medical University) Juanfen Li (The Affiliated Hospital of Guilin Medical University)

저널정보: 대한심장학회 Korean Circulation Journal Korean Circulation Journal Vol.53 No.3

발행연도: 2023.3

수록면: 151 - 167 (17page)

DOI: https://doi.org/10.4070/kcj.2022.0242

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Background and Objectives: Acute myocardial infarction (AMI) often occurs suddenly and leads to fatal consequences. Ferroptosis is closely related to the progression of AMI. However, the specific mechanism of ferroptosis in AMI remains unclear. Methods: We constructed a cell model of AMI using AC16 cells under oxygen and glucose deprivation (OGD) conditions and a mice model of AMI using the left anterior descending (LAD) ligation. The 3-(4, 5-dimethylthiazol-2-yl)-2, 5 diphenyltetrazolium bromide was employed to determine cell viability. The levels of lactate dehydrogenase, creatine kinase, reactive oxygen species (ROS), glutathione (GSH), malondialdehyde (MDA), and iron were measured using corresponding kits. Dual luciferase reporter gene assay, RNA-binding protein immunoprecipitation, and RNA pull-down were performed to validate the correlations among AC005332.7, miR-331-3p, and cyclin D2 (CCND2). Hematoxylin and eosin staining was employed to evaluate myocardial damage. Results: AC005332.7 and CCND2 were lowly expressed, while miR-331-3p was highly expressed in vivo and in vitro models of AMI. AC005332.7 sufficiency reduced ROS, MDA, iron, and ACSL4 while boosting the GSH and GPX4, indicating that AC005332.7 sufficiency impeded ferroptosis to improve cardiomyocyte injury in AMI. Mechanistically, AC005332.7 interacted with miR-331-3p, and miR-331-3p targeted CCND2. Additionally, miR-331-3p overexpression or CCND2 depletion abolished the suppressive impact of AC005332.7 on ferroptosis in OGD-induced AC16 cells. Moreover, AC005332.7 overexpression suppressed ferroptosis in mice models of AMI. Conclusions: AC005332.7 suppressed ferroptosis in OGD-induced AC16 cells and LAD ligation-operated mice through modulating miR-331-3p/CCND2 axis, thereby mitigating the cardiomyocyte injury in AMI, which proposed novel targets for AMI treatment.

#Myocardial infarction #lncRNA #MicroRNA #Cyclin D2 #Ferroptosis

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