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CircSAMD4A aggravates H/R-induced cardiomyocyte apoptosis and inflammatory response by sponging miR-138-5p
Xiaorong Hu1, Ruisong Ma2, Jianlei Cao1
1Department of Cardiology, Zhongnan Hospital of Wuhan University, Wuhan, China.
Insights
Circular SAMD4A (circSAMD4A) exacerbates myocardial cell injury from hypoxia/reoxygenation by suppressing miR-138-5p. Inhibiting circSAMD4A reduces apoptosis and inflammation in acute myocardial infarction models.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- RNA Biology
Background:
- Hypoxia/reoxygenation (H/R) injury is a primary cause of acute myocardial infarction (AMI).
- Circular RNAs (circRNAs) are increasingly recognized for their roles in cardiovascular diseases, including AMI.
- Understanding the specific functions of circRNAs in H/R-induced myocardial injury is crucial for developing therapeutic strategies.
Purpose of the Study:
- To investigate the role of circSAMD4A in H/R-induced myocardial cell injury.
- To explore the regulatory relationship between circSAMD4A and miR-138-5p in the context of myocardial injury.
Main Methods:
- Quantification of circSAMD4A and miR-138-5p levels using real-time quantitative PCR.
- Assessment of cell viability, apoptosis (TUNEL, Annexin V-FITC), and inflammatory markers (IL-1β, TNF-α, IL-6) via MTT assay, flow cytometry, and ELISA kits.
- Western blot analysis to detect apoptosis-related proteins (Bcl-2, Bax).
Main Results:
- circSAMD4A levels were significantly upregulated in H/R-induced myocardial injury models (both in vivo and in vitro).
- Inhibition of circSAMD4A attenuated H/R-induced myocardial cell apoptosis and inflammation.
- circSAMD4A was found to directly target and downregulate miR-138-5p, a microRNA that was suppressed by H/R.
- Overexpression of circSAMD4A promoted H/R-induced myocardial cell injury, while miR-138-5p inhibition reversed this effect.
Conclusions:
- circSAMD4A acts as a crucial mediator in H/R-induced myocardial injury.
- circSAMD4A promotes myocardial cell apoptosis and inflammation by sponging miR-138-5p.
- circSAMD4A represents a potential therapeutic target for mitigating H/R-induced myocardial damage in AMI.
Abstract:
Hypoxia/reoxygenation (H/R)-induced myocardial cell injury is the main cause of acute myocardial infarction (AMI). Many proofs show that circular RNA plays an important role in the development of AMI. The purpose of this study was to investigate the role of circSAMD4A in H/R-induced myocardial injury. The levels of circular SAMD4A (circSAMD4A) were detected in the heart tissues of AMI mice and H/R-induced H9C2 cells, and the circSAMD4A was suppressed in AMI mice and H/R-induced H9C2 cells to investigate its' function in AMI. The levels of circSAMD4A and miR-138-5p were detected by real-time quantitative PCR, and MTT assay was used to detect cell viability. TUNEL analysis and Annexin V-FITC were used to determine apoptosis. The expression of Bcl-2 and Bax proteins was detected by Western blot. IL-1β, TNF-α and IL-6 were detected by ELISA kits. The study found that the levels of circSAMD4A were up-regulated after H/R induction and inhibition of circSAMD4A expression would reduce the H/R-induced apoptosis and inflammation. MiR-138-5p was down-regulated in H/R-induced H9C2 cells. circSAMD4A was a targeted regulator of miR-138-5p. CircSAMD4A inhibited the expression of miR-138-5p to promote H/R-induced myocardial cell injury in vitro and vivo. In conclusion, CircSAMD4A can sponge miR-138-5p to promote H/R-induced apoptosis and inflammatory response.
