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The diagnostic and functional values of circFOXP1 in acute myocardial infarction
Zheyi Rong1, Jingyi Yan2, Junbo Wei3
1Department of Cardiovascular Medicine, Renhe Hospital of Baoshan District, Shanghai, China.
Insights
Circular RNAs (circRNAs) are downregulated in acute myocardial infarction (AMI) patients. circFOXP1 acts as a diagnostic marker and suppresses apoptosis, inflammation, and oxidative stress via miR-9-3p.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Biomarker Discovery
Background:
- Circular RNAs (circRNAs) play a role in the pathogenesis of acute myocardial infarction (AMI).
- circFOXP1 is investigated for its potential diagnostic and functional significance in AMI.
Purpose of the Study:
- To evaluate circFOXP1 as a diagnostic marker for AMI.
- To elucidate the functional role of circFOXP1 in AMI pathogenesis.
Main Methods:
- circFOXP1 expression analyzed by RT-qPCR and ROC curve analysis.
- Luciferase reporter assay to identify circFOXP1's target gene.
- In vitro (AC16 cells) and in vivo (mice) AMI models used to assess proliferation, apoptosis, inflammation, and oxidative stress.
Main Results:
- circFOXP1 expression is significantly downregulated in AMI patients.
- circFOXP1 overexpression reduces apoptosis, inflammation (TNF-α, IL-1β, IL-6), and oxidative stress (ROS, LDH) while increasing GSH.
- miR-9-3p identified as a direct target of circFOXP1 and mediates its effects.
Conclusions:
- circFOXP1 serves as a potential diagnostic biomarker for AMI.
- Overexpression of circFOXP1 mitigates apoptosis, inflammation, and oxidative stress in AMI models through the miR-9-3p pathway.
Background:
Circular RNAs (circRNAs) are implicated in the pathogenesis of acute myocardial infarction (AMI). Current research aims to evaluate the diagnostic and functional value of circFOXP1 in AMI patients.
Methods:
The expression of circFOXP1 was assessed using RT-qPCR, and its diagnostic potential was determined through receiver operating characteristic (ROC) curve. The target gene of circFOXP1 was identified using a luciferase reporter assay. An in vitro hypoxia/reoxygenation (H/R) model was established in AC16 cells, while an AMI model was constructed in C57BL/6 mice. The proliferation and apoptosis of AC16 cells were evaluated using CCK8 and flow cytometry (FCM). The impact of circFOXP1 on inflammation was measured by assessing levels of TNF-α, IL-1β, and IL-6, while the effects of circFOXP1 on oxidative stress were evaluated through measurements of reactive oxygen species (ROS), glutathione (GSH), and lactate dehydrogenase (LDH) levels.
Results:
circFOXP1 expression was found to be downregulated in AMI patients compared to controls. The ROC curve indicated an area under the curve (AUC) was 0.881 (95%CI=0.847-0.915), with a sensitivity of 0.930 and a specificity of 0.785. Additionally, miR-9-3p was identified as a direct target gene of circFOXP1. High levels of circFOXP1 did not significantly affect f the proliferation of H/R stimulated AC16 cells; however, increased circFOXP1 resulted in significant reduction in cell apoptosis (P<0.001). TNF-α, IL-1β, and IL-6 levels were significantly lower in pcDNA3.1-circFOXP1-transfected cells (P<0.001). ROS concentration and LDH level were markedly reduced in these cells (P<0.01), while GSH level (P<0.001) was significantly elevated. miR-9-3p, as a direct target gene of circFOXP1, was found to reverse the effects of circFOXP1 on H/R AC16 cells and AMI model.
Conclusions:
circFOXP1 was decreased in AMI patients and may serve as a diagnostic marker for AMI. Overexpression of circFOXP1 was shown to suppress apoptosis, inflammation, and oxidative stress via miR-9-3p in AC16 cells and the AMI model.
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