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Circular RNA ANKIB1 alleviates hypoxia-induced cardiomyocyte injury by modulating miR-452-5p/SLC7A11 axis
Gang Li1, Xiaolei Tang2, Huaping Tang1
1Department of Geriatric Medicine, Maanshan People's Hospital, China.
Insights
Circular RNA circANKIB1 protects heart cells from damage caused by low oxygen. It achieves this by regulating the miR-452-5p/SLC7A11 pathway, offering a potential new treatment for acute myocardial infarction.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- RNA Biology
Background:
- Acute myocardial infarction (AMI) is a significant global health concern.
- Circular RNAs (circRNAs) play crucial roles in AMI pathogenesis.
- The specific role of circANKIB1 in hypoxia-induced cardiomyocyte injury remains largely unknown.
Purpose of the Study:
- To investigate the protective function of circANKIB1 against hypoxia-induced cardiomyocyte injury.
- To elucidate the underlying molecular mechanisms involving circANKIB1 in AMI.
Main Methods:
- Quantitative real-time PCR and Western blot analysis for gene and protein expression.
- MTT and TUNEL assays to assess cell viability and apoptosis.
- Measurement of reactive oxygen species (ROS), ferrous ion (Fe2+), and malondialdehyde (MDA) levels.
- Dual luciferase reporter assays to validate circANKIB1 and miR-452-5p interactions.
Main Results:
- circANKIB1 expression decreased under hypoxia; its overexpression reversed hypoxia-induced cell damage, reduced apoptosis, and normalized oxidative stress markers.
- circANKIB1 directly targets miR-452-5p, which in turn targets SLC7A11.
- The miR-452-5p/SLC7A11 axis mediates the protective effects of circANKIB1 against hypoxia.
Conclusions:
- circANKIB1 ameliorates hypoxia-induced cardiomyocyte injury by regulating the miR-452-5p/SLC7A11 signaling pathway.
- circANKIB1 presents a potential therapeutic target for treating acute myocardial infarction.
Background:
Acute myocardial infarction (AMI) is a common cardiovascular disease worldwide. Circular RNAs (circRNAs) have been shown to exert essential roles in the progression of AMI. However, it remains unclear whether circANKIB1 protects cardiomyocytes from hypoxia-induced injury.
Objectives:
The aim of the study was to elucidate the function and mechanisms of circANKIB1 in AMI.
Material And Methods:
The expression of RNA was estimated using a quantitative real-time polymerase chain reaction (qPCR) assay, and the level of protein was determined with the use of western blot analysis. Methyl thiazolyl tetrazolium (MTT) assay was introduced to test cell viability, and a terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay was used to detect apoptosis. The relative levels of ferrous ion (Fe2+), reactive oxygen species (ROS) and malondialdehyde (MDA) were measured with their corresponding detection kits. The potential target of circANKIB1 and miR-452-5p was predicted using the StarBase database and verified by employing a dual luciferase reporter assay.
Results:
This study showed a significant decrease in circANKIB1 in hypoxia-treated H9c2 cells. Hypoxic exposure significantly reduced the viability of H9c2 cells and the expression of GPX4, and increased the content of Fe2+, ROS and MDA. These effects were reversed by the overexpression of circANKIB1. Additionally, miR-452-5p was found to be a direct target of circANKIB1, and the miR-452-5p mimic significantly eliminated the protective effect of circANKIB1 overexpression in hypoxia-induced cells. In addition, miR-452-5p could bind to SLC7A11 and negatively regulate its expression. The knockdown of SLC7A11 abolished the effect of circANKIB1 overexpression on hypoxia-induced cardiomyocyte injury.
Conclusions:
This investigation revealed for the first time that circANKIB1 regulated signaling of the miR-452-5p/SLC7A11 axis, thereby ameliorating hypoxia-induced cardiomyocyte injury. These findings suggest that circANKIB1 might be a useful adjunct in the treatment of AMI.
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