Related Experiment Video
Updated: Apr 25, 2026
Induction of Myocardial Infarction and Myocardial Ischemia-Reperfusion Injury in Mice
Published on: January 19, 2022
Induction of myocardial PDCD4 in coronary microembolization-related cardiac dysfunction: evidence from a large-animal
1Department of Cardiology, the First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Background/Aims:
Coronary microembolization (CME) has been linked to myocardial inflammation and apoptosis. This study aims to investigate the role of the apoptotic protein PDCD4 in the myocardium after CME in minipigs.
Methods:
Seventy Bama minipigs were randomized into four groups: control, CME, CME plus PDCD4-siRNA and CME plus control siRNA. CME was induced by injecting polyethylene microspheres into the left anterior descending artery. Cardiac function was evaluated. HE and HBFP staining were used to observe the degree of infarction. Western blotting and qPCR were used to evaluate the expression of PDCD4, TNF-α and caspase-3. The measurements were performed at 0, 3, 6, 9, 12 and 24 h after CME modeling in the CME and control groups.
Results:
Cardiac function in the CME group was significantly decreased compared with the control group (P<0.05) and the expression of PDCD4 and TNF-α increased significantly (P<0.05). However, the infarct area did not differ between the CME and control groups at any time point (P>0.05). Furthermore, PDCD4-siRNA improved cardiac function and reduced PDCD4 and TNF-α expression compared with the CME plus control siRNA group at 9 h after modeling (P < 0.05), while the caspase-3 level was not different between the two groups.
Conclusion:
PDCD4 induction may be involved in CME-related cardiac dysfunction, and PDCD4 inhibition via siRNA may attenuate the cardiac impairment and be used as a treatment strategy for CME.
Insights
Coronary microembolization (CME) impairs cardiac function and increases programmed cell death protein 4 (PDCD4). Inhibiting PDCD4 with siRNA improved heart function in a minipig model of CME.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Cell Death Mechanisms
Background:
- Coronary microembolization (CME) is associated with myocardial inflammation and apoptosis.
- The role of programmed cell death protein 4 (PDCD4) in CME-induced cardiac dysfunction remains unclear.
Purpose of the Study:
- To investigate the role of PDCD4 in the myocardium following coronary microembolization (CME) in a minipig model.
- To evaluate the therapeutic potential of inhibiting PDCD4 in CME.
Main Methods:
- Minipigs underwent coronary microembolization (CME) or were assigned to control groups.
- Cardiac function, infarct size, and expression of PDCD4, TNF-α, and caspase-3 were assessed.
- PDCD4 expression was inhibited using small interfering RNA (siRNA) in a subset of CME pigs.
Main Results:
- CME significantly decreased cardiac function and increased PDCD4 and TNF-α expression.
- No significant difference in infarct area was observed between CME and control groups.
- PDCD4 inhibition via siRNA improved cardiac function and reduced PDCD4 and TNF-α levels at 9 hours post-CME.
Conclusions:
- PDCD4 plays a role in CME-induced cardiac dysfunction.
- Inhibiting PDCD4 may serve as a potential therapeutic strategy for treating coronary microembolization.
