Related Experiment Video
Updated: Feb 4, 2026
Enhancing the Engraftment of Human Induced Pluripotent Stem Cell-derived Cardiomyocytes via a Transient Inhibition of Rho Kinase Activity
Published on: July 10, 2019
MiR-223 promotes cardiomyocyte apoptosis by inhibiting Foxo3a expression
1Department of Nursing, Medical College, Hebei University of Engineering, Handan, Hebei, China.wangpeipei19@126.com.
Objective:
MicroRNAs (miRs) are proven to possess diversified functions in the pathogenesis of cardiac diseases. The current study is designed aiming at determining the effect of miR-223 on oxidative stress induced apoptosis in cardiomyocytes.
Materials And Methods:
Mouse model of myocardial infarction (MI) was constructed, and endogenous level of miR-223 in the border zone of infarcted heart tissues was determined. Primarily cultured cardiomyocytes were exposed to H2O2 treatment to mimic the oxidative stress stimulation. Multiple approaches including quantitative reverse transcription polymerase chain reaction (qRT-PCR), cell viability assay, luciferase assay, Western blot assay and flow cytometry assay were employed to determine its expression, function and mechanism in apoptosis.
Results:
MiR-223 expression was significantly upregulated in the border zone of infarcted heart ventricular tissues and in cardiomyocytes treated with H2O2. Overexpression of miR-223 in cardiomyocytes promoted apoptosis, whereas inhibition of endogenous miR-223 protected cardiomyocytes from oxidative stress induced apoptosis. MiR-223 directly targets the 3'untranslated region (UTR) of Foxo3a mRNA. Overexpression of miR-223 inhibited Foxo3a protein expression, however, inhibition of miR-223 suppressed its expression. Silencing Foxo3a using small interfering RNA (siRNA) mimicked the effect of miR-223, indicating its functional significance.
Conclusions:
MiR-223 is an important regulator of cardiomyocyte apoptosis under oxidative stress. Inhibition of the miR-223/Foxo3a signaling axis may be a potential therapeutic strategy for cardiac injuries.
Insights
MicroRNA-223 (miR-223) promotes apoptosis in cardiomyocytes during oxidative stress. Inhibiting the miR-223/Foxo3a pathway may offer a therapeutic approach for cardiac injuries.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Cellular Stress Response
Background:
- MicroRNAs (miRs) play critical roles in cardiovascular disease pathogenesis.
- Oxidative stress is a key factor in cardiomyocyte apoptosis and cardiac dysfunction.
Purpose of the Study:
- To investigate the role of miR-223 in oxidative stress-induced apoptosis in cardiomyocytes.
- To elucidate the underlying molecular mechanism involving the miR-223/Foxo3a axis.
Main Methods:
- Construction of a mouse model of myocardial infarction (MI).
- Primary cardiomyocyte culture subjected to hydrogen peroxide (H2O2) treatment.
- Quantitative reverse transcription polymerase chain reaction (qRT-PCR), cell viability assays, luciferase assays, Western blotting, and flow cytometry were utilized.
Main Results:
- miR-223 expression was significantly upregulated in infarcted heart tissues and H2O2-treated cardiomyocytes.
- miR-223 overexpression promoted apoptosis, while inhibition protected against oxidative stress-induced cell death.
- miR-223 directly targets Foxo3a mRNA, inhibiting its protein expression. Silencing Foxo3a mimicked miR-223 effects.
Conclusions:
- miR-223 acts as a significant regulator of cardiomyocyte apoptosis under oxidative stress conditions.
- Targeting the miR-223/Foxo3a signaling pathway presents a potential therapeutic strategy for managing cardiac injuries.
More Related Videos
09:34Identification of Growth Inhibition Phenotypes Induced by Expression of Bacterial Type III Effectors in Yeast
Published on: March 30, 2010
10:05Improved Generation of Induced Cardiomyocytes Using a Polycistronic Construct Expressing Optimal Ratio of Gata4, Mef2c and Tbx5
Published on: November 13, 2015
Related Concept Videos
02:40The Eukaryotic Promoter Region
02:40The Eukaryotic Promoter Region
01:30Apoptosis
00:46Feedback Inhibition
01:42What is Gene Expression?
Gene expression is the process in which DNA directs the synthesis of functional products, that is, proteins. Cells can regulate gene expression at various stages. It allows organisms to generate different cell types and enables cells to adapt to internal and external factors.
Genetic Information Flows from DNA to RNA to Protein
A gene is a stretch of DNA that serves as the blueprint for functional RNAs and proteins. Since DNA is made up of nucleotides and proteins consist of amino...
01:30Enzyme Inhibition