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Transplantation of Neonatal Mouse Cardiac Macrophages into Adult Mice
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Nucleolin Improves Heart Function During Recovery From Myocardial Infarction by Modulating Macrophage Polarization
Yuting Tang1,2, Xiaofang Lin1,2, Cheng Chen1,2
1Department of Pathophysiology, Xiangya School of Medicine, 12570Central South University, Changsha, Hunan, China.
Journal of Cardiovascular Pharmacology and Therapeutics
|February 8, 2021
Summary
Nucleolin deficiency impairs heart recovery after myocardial infarction (MI) by reducing M2 macrophage polarization. This suggests nucleolin as a potential therapeutic target for ischemic heart disease.
Area of Science:
- Cardiovascular Biology
- Cellular Mechanisms
- Immunology
Background:
- Nucleolin plays a role in cell survival and proliferation.
- Previous studies show nucleolin reduces myocardial ischemia-reperfusion injury.
- Nucleolin promotes angiogenesis and reduces apoptosis in the heart.
Purpose of the Study:
- To investigate the role of nucleolin in myocardial infarction (MI) injury recovery.
- To elucidate the underlying mechanisms of nucleolin's function in MI recovery.
Main Methods:
- Myocardial infarction (MI) models were created in male BALB/c mice.
- Nucleolin expression was downregulated using lentiviral vectors with small interfering RNA.
- Macrophage infiltration and polarization, and cytokine levels were analyzed.
Main Results:
- Nucleolin expression decreased early and increased late after MI.
- Nucleolin knockdown impaired heart function and survival post-MI.
- Nucleolin knockdown reduced M2 macrophage polarization, a key factor in heart repair.
Conclusions:
- Nucleolin deficiency hinders heart recovery post-MI by reducing M2 macrophage polarization.
- Targeting nucleolin may offer a novel therapeutic strategy for ischemic heart disease.
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