The apolipoprotein a-i mimetic l-4f attenuates monocyte activation and adverse cardiac remodeling after myocardial infarction

Tariq Hamid, Mohamed Ameen Ismahil, Shyam S. Bansal, Bindiya Patel, Mehak Goel, C. Roger White, G. M. Anantharamaiah, Sumanth D. Prabhu

Research output: Contribution to journalArticlepeer-review

3 Scopus citations

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.

Original languageEnglish
Article number3519
JournalInternational journal of molecular sciences
Volume21
Issue number10
DOIs
StatePublished - May 2 2020

Keywords

  • Cardiac remodeling
  • Heart failure
  • Inflammation
  • Macrophage polarity

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