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The Apolipoprotein A-I Mimetic L-4F Attenuates Monocyte Activation and Adverse Cardiac Remodeling after Myocardial
Tariq Hamid1, Mohamed Ameen Ismahil1, Shyam S Bansal1
1Division of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL 35233, USA.
Abstract:
Excessive inflammation after myocardial infarction (MI) can promote infarct expansion and adverse left ventricular (LV) remodeling. L-4F, a mimetic peptide of apolipoprotein A-I (apoA-I), exhibits anti-inflammatory and anti-atherogenic properties; however, whether L-4F imparts beneficial effects after myocardial infarction (MI) is unknown. Here we demonstrate that L-4F suppresses the expansion of blood, splenic, and myocardial pro-inflammatory monocytes and macrophages in a mouse model of reperfused MI. Changes in immune cell profiles were accompanied by alleviation of post-MI LV remodeling and dysfunction. In vitro, L-4F also inhibited pro-inflammatory and glycolytic gene expression in macrophages. In summary, L-4F treatment prevents prolonged and excessive inflammation after MI, in part through modulation of pro-inflammatory monocytes and macrophages, and improves post-MI LV remodeling. These data suggest that L-4F could be a used as a therapeutic adjunct in humans with MI to limit inflammation and alleviate the progression to heart failure.
Insights
L-4F peptide reduces harmful inflammation and improves heart function after myocardial infarction (MI) in mice. This peptide therapy limits immune cell expansion, preventing adverse cardiac remodeling and potentially aiding heart failure treatment.
Area of Science:
- Cardiovascular Research
- Immunology
- Pharmacology
Background:
- Excessive inflammation post-myocardial infarction (MI) exacerbates cardiac damage and left ventricular (LV) remodeling.
- The peptide L-4F, derived from apolipoprotein A-I (apoA-I), is known for anti-inflammatory and anti-atherogenic effects.
Purpose of the Study:
- To investigate the therapeutic potential of L-4F in mitigating post-MI inflammation and adverse cardiac remodeling.
- To determine if L-4F influences immune cell profiles and gene expression in the context of MI.
Main Methods:
- Utilized a mouse model of reperfused myocardial infarction (MI).
- Administered L-4F peptide and assessed immune cell populations (monocytes, macrophages) in blood, spleen, and heart.
- Evaluated left ventricular (LV) remodeling and function post-MI.
- Performed in vitro studies on macrophage gene expression (pro-inflammatory and glycolytic pathways).
Main Results:
- L-4F treatment significantly suppressed pro-inflammatory monocyte and macrophage expansion in blood, spleen, and myocardium.
- Observed alleviation of adverse LV remodeling and improved cardiac function following L-4F administration.
- In vitro, L-4F inhibited pro-inflammatory and glycolytic gene expression in macrophages.
Conclusions:
- L-4F effectively prevents excessive post-MI inflammation by modulating pro-inflammatory monocytes and macrophages.
- L-4F treatment improves cardiac remodeling and function after myocardial infarction.
- L-4F shows promise as a therapeutic agent to limit inflammation and prevent heart failure progression in MI patients.
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