Abstract 358: Myeloid-specific Il-4 Receptor α Knockout Alters Cardiac Remodeling Post-myocardial Infarction

• DOI: 10.1161/atvb.36.suppl_1.358
• Publication Date: 2021-06-21T16:58:35Z
• Authors: Jianrui Song; Thomas Vigil; Yutein Chung; Ryan Frieler; Sascha Goonewardena; Richard Mortensen
• Keywords: Ventricular remodeling; Knockout mouse

Introduction: Cardiac remodeling post myocardial infarction (MI) can be a critical determinant of outcome for patients with MI. Well-contained inflammation results in successful infarct healing while excessive cause adverse which leads to heart failure. Macrophages are important participants inflammation, helping resolve pro-inflammatory reactions and performing reparative processes. Reprogramming macrophages towards resolving phenotype is potential therapeutic approach. We hypothesized that IL4/IL13-induced, alternatively activated (M2) have an role cardiac post-MI, we tested this hypothesis mouse model MI using myeloid-specific IL4 receptor α knockout mice (MyIL4RaKO). Methods: MyIL4RaKO were generated IL4Ra flox/flox ;LysM-Cre. was induced by ligating the left anterior descending coronary artery. Hearts cut into 1mm sections, then stained tetrazolium chloride size measurement. Evenly spaced radians taken through center ventricle 5μm average thickness calculated. qPCR used determine gene expression. Echocardiography performed at baseline 3 weeks Results: Initial not affected but 1-week MI, (16.54 ± 2.433, n=11) shown significantly smaller than FC (24.96 2.005, n=15) showing changes (p= 0.0129). Changes continued 3-week (0.2171 0.01053, n=6) increased, compared (0.3508 0.03629, n=8, p= 0.0094). These accompanied also showed lower level fibrosis markers: Col1A1 Plod2. A ejection fraction observed (25.46 3.749, n=5) (37.90 2.309, 0.0223). Conclusions: Myeloid-specific alteration remodeling, altered decreased function although hypertrophy did show significant change.