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Updated: Oct 11, 2025
Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury
Published on: March 7, 2022
miR-190-5p Alleviates Myocardial Ischemia-Reperfusion Injury by Targeting PHLPP1
Yangxue Li1, Zhibo Li1, Jiangen Liu1
1Department of Cardiology, The Second Hospital of Jilin University, Changchun, China.
Objective:
Myocardial ischemia-reperfusion (I/R) injury (MIRI) refers to the more serious myocardial injury after blood flow recovery, which seriously affects the prognosis of patients with ischemic cardiomyopathy. This study explored the new targets for MIRI treatment by investigating the effects of miR-190-5p and its downstream target on the structure and function of myocardial cells.
Methods:
We injected agomir miR-190-5p into the tail vein of rats to increase the expression of miR-190-5p in rat myocardial cells and made an I/R rat model by coronary artery occlusion. We used 2,3,5-triphenyl tetrazolium chloride staining, lactate dehydrogenase (LDH) detection, echocardiography, and hematoxylin-eosin (HE) staining to determine the degree of myocardial injury in I/R rats. In addition, we detected the expression of inflammatory factors and apoptosis-related molecules in rat serum and myocardial tissue to determine the level of inflammation and apoptosis in rat myocardium. Finally, we determined the downstream target of miR-190-5p by Targetscan system and dual luciferase reporter assay.
Results:
The expression of miR-190-5p in an I/R rat myocardium was significantly lower than that in normal rats. After treatment of I/R rats with agomir miR-190-5p, the ischemic area of rat myocardium and the concentration of LDH decreased. The results of echocardiography and HE staining also found that overexpression of miR-190-5p improved the structure and function of rat myocardium. miR-190-5p was also found to improve the viability of H9c2 cells in vitro and reduce the level of apoptosis of H9c2 cells. The results of Targetscan system and dual luciferase reporter assay found that miR-190-5p targeted to inhibit pleckstrin homology domain leucine-rich repeat protein phosphatase 1 (PHLPP1). In addition, inhibition of PHLPP1 was found to improve the viability of H9c2 cells.
Conclusion:
Therefore, miR-190-5p can reduce the inflammation and apoptosis of myocardium by targeting PHLPP1, thereby alleviating MIRI.
Insights
MicroRNA-190-5p (miR-190-5p) protects against myocardial ischemia-reperfusion injury (MIRI) by targeting PHLPP1. This study demonstrates miR-190-5p as a potential therapeutic target for MIRI.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- MicroRNA Therapeutics
Background:
- Myocardial ischemia-reperfusion injury (MIRI) significantly worsens outcomes for patients with ischemic cardiomyopathy.
- Identifying novel therapeutic targets is crucial for mitigating MIRI and improving patient prognosis.
Purpose of the Study:
- To investigate the therapeutic potential of miR-190-5p and its downstream targets in alleviating MIRI.
- To explore the effects of miR-190-5p on myocardial cell structure and function.
Main Methods:
- An MIRI rat model was established, and miR-190-5p expression was modulated using agomir injections.
- Myocardial injury, inflammation, and apoptosis were assessed using biochemical assays, echocardiography, and histological staining.
- Downstream targets of miR-190-5p were identified via Targetscan and dual luciferase reporter assays.
Main Results:
- miR-190-5p expression was downregulated in MIRI rat myocardium.
- Overexpression of miR-190-5p reduced infarct size, lactate dehydrogenase levels, and improved cardiac function and structure in MIRI rats.
- miR-190-5p enhanced H9c2 cell viability and reduced apoptosis, targeting PHLPP1 for inhibition.
Conclusions:
- miR-190-5p alleviates MIRI by targeting and inhibiting PHLPP1, thereby reducing myocardial inflammation and apoptosis.
- miR-190-5p represents a promising therapeutic strategy for treating MIRI.
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