The Apolipoprotein A-I Mimetic L-4F Attenuates Monocyte Activation and Adverse Cardiac Remodeling after Myocardial Infarction

Autor: Mehak Goel, Bindiya Patel, Shyam S. Bansal, Mohamed Ameen Ismahil, C. Roger White, Gattadahalli M. Anantharamaiah, Tariq Hamid, Sumanth D. Prabhu
Jazyk: angličtina
Rok vydání: 2020
Předmět:
0301 basic medicine
Male
Apolipoprotein B
Cell
Cell Plasticity
Myocardial Infarction
heart failure
030204 cardiovascular system & hematology
macrophage polarity
Monocytes
lcsh:Chemistry
Mice
Ventricular Dysfunction
Left
0302 clinical medicine
Glycolysis
Myocardial infarction
lcsh:QH301-705.5
Spectroscopy
biology
Ventricular Remodeling
General Medicine
Computer Science Applications
medicine.anatomical_structure
Cardiology
cardiovascular system
lipids (amino acids
peptides
and proteins)
medicine.symptom
medicine.medical_specialty
Systole
Inflammation
Catalysis
Article
Inorganic Chemistry
03 medical and health sciences
Immune system
Internal medicine
medicine
Animals
cardiovascular diseases
Physical and Theoretical Chemistry
Molecular Biology
Apolipoprotein A-I
business.industry
Monocyte
Macrophages
Organic Chemistry
Macrophage Activation
medicine.disease
Mice
Inbred C57BL
030104 developmental biology
RAW 264.7 Cells
lcsh:Biology (General)
lcsh:QD1-999
inflammation
Heart failure
biology.protein
cardiac remodeling
business
Peptides
Zdroj: International Journal of Molecular Sciences
Volume 21
Issue 10
International Journal of Molecular Sciences, Vol 21, Iss 3519, p 3519 (2020)
ISSN: 1422-0067
DOI: 10.3390/ijms21103519
Popis: 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.
Databáze: OpenAIRE
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