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An Experimental Model of Myocardial Infarction for Studying Cardiac Repair and Remodeling in Knockout Mice
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CD226 deletion improves post-infarction healing via modulating macrophage polarization in mice
Jun Li1, Yun Song2, Jing-Yi Jin2
1Department of Physiology and Pathophysiology, National Key Discipline of Cell Biology, School of Basic Medicine, Fourth Military Medical University, No.169, West Changle Road, Xi'an, 710032, China.
Theranostics
|February 28, 2020
Summary
Inhibiting CD226 improves heart repair after myocardial infarction (MI) by promoting beneficial M2 macrophages and reducing harmful M1 macrophages, enhancing cardiac function and wound healing.
Area of Science:
- Cardiovascular Biology
- Immunology
- Regenerative Medicine
Background:
- Macrophages are crucial for healing after myocardial infarction (MI).
- The role of CD226 in infarct healing and its effect on macrophages were previously unknown.
Purpose of the Study:
- To investigate the role of CD226 in post-myocardial infarction (MI) cardiac wound healing.
- To determine the effect of CD226 deletion on macrophage polarization and cardiac repair.
Main Methods:
- Mice lacking CD226 (CD226 KO) and wild-type mice underwent permanent coronary ligation to model MI.
- Cardiac function, ventricular remodeling, macrophage profiles (M1/M2), myofibroblasts, angiogenesis, and monocyte mobilization were assessed.
- In vitro studies examined CD226's effect on bone marrow-derived macrophage polarization.
Main Results:
- CD226 expression increased in the infarcted heart post-MI.
- CD226 deletion attenuated infarct expansion, improved healing, and enhanced cardiac function.
- CD226 deficiency promoted M2 macrophage accumulation and M1 macrophage reduction, increased myofibroblasts and angiogenesis, and reduced inflammatory monocyte mobilization.
Conclusions:
- CD226 is upregulated in infarcted hearts and negatively impacts healing.
- Deleting CD226 promotes reparative macrophage polarization, improves cardiac function, and enhances wound healing after MI.
- CD226 inhibition offers a potential therapeutic strategy for improving outcomes post-MI.
