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Published on: January 10, 2025
Potential Involvement of MiR-30e-3p in Myocardial Injury Induced by Coronary Microembolization via Autophagy
Background/Aims:
Coronary microembolization (CME) can lead to no-reflow or slow reflow, which is one of the important reasons for loss of clinical benefit from myocardial reperfusion therapy. MicroRNAs and autophagy are heavily implicated in the occurrence and development of almost all cardiovascular diseases. Therefore, the present study was designed to investigate the role of miR-30e-3p and autophagy in CME-induced myocardial injury rat model.
Methods:
Sixty rats were randomly divided into six groups: sham, CME 1h,3h,6h,9h, and 12h (n = 10 per group). Our CME rat model was created by injecting polyethylene microspheres (42mm) into the left ventricle of the heart; the sham group was injected with same volume of normal saline. The cardiac function and serum cardiac troponin I (cTnI) level of each group was measured. HE staining and HBFP staining were used to evaluate the myocardial micro-infarction area of myocardium tissue samples. Then RT-qPCR and western blot were used to detect the expression of miR-30e-3p and, autophagy related protein LC3-II and p62, respectively. Transmission electron microscope (TEM) was used to identify autophagic vacuoles in tissue samples.
Results:
The cardiac function of the CME 6h,9h, and 12h groups were significantly decreased compared to the sham group (P < 0.05) and the cTnI level in each group were also significantly increased (P < 0.05). The expression of miR-30e-3p in the CME 6h, 9h and 12h group were decreased significantly compared with the sham group (P < 0.05). Meanwhile, the expression of autophagy related protein LC3-II decreased significantly and p62 increased significantly in the CME 9h and 12h group (P < 0.05). TEM images showed typical autophagic vacuoles for each of the CME groups.
Conclusions:
Myocardial miR-30e-3p is down regulated after CME and is accompanied by inhibited autophagy and decreased cardiac function. Therefore, miR-30e-3p may be involved in CME-induced cardiac dysfunction by regulating myocardial autophagy.
Insights
Coronary microembolization (CME) in rats reduced miR-30e-3p levels and inhibited autophagy, leading to impaired cardiac function. This suggests miR-30e-3p plays a role in CME-induced heart damage by affecting autophagy.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Cellular Biology
Background:
- Coronary microembolization (CME) impairs myocardial reperfusion therapy outcomes.
- MicroRNAs and autophagy are critical in cardiovascular disease pathogenesis.
- Understanding their roles in CME is vital for therapeutic advancements.
Purpose of the Study:
- To investigate the role of miR-30e-3p and autophagy in a rat model of CME-induced myocardial injury.
- To determine the relationship between miR-30e-3p expression, autophagy, and cardiac dysfunction following CME.
Main Methods:
- A rat model of coronary microembolization was established using polyethylene microspheres.
- Cardiac function, serum cardiac troponin I, and myocardial micro-infarction were assessed.
- Expression of miR-30e-3p, LC3-II, and p62 was analyzed using RT-qPCR and Western blot.
- Autophagic vacuoles were identified via transmission electron microscopy.
Main Results:
- CME significantly decreased cardiac function and increased cardiac troponin I levels in a time-dependent manner.
- Downregulation of miR-30e-3p was observed in CME groups compared to sham.
- Inhibited autophagy, indicated by decreased LC3-II and increased p62, was evident in later CME groups.
- TEM confirmed the presence of autophagic vacuoles in CME-induced myocardial injury.
Conclusions:
- Myocardial miR-30e-3p is downregulated following CME, coinciding with inhibited autophagy and reduced cardiac function.
- miR-30e-3p may contribute to CME-induced cardiac dysfunction by modulating myocardial autophagy.
