The role of α5 Integrin in regulating macrophage phenotype and function during cardiac remodeling after myocardial infarction. The role of α5 Integrin in regulating macrophage phenotype and function during cardiac remodeling after myocardial infarction

Macrophages infiltrate the infarcted heart and play a critical role in repair, remodeling and fibrosis. Macrophages sense changes in the extracellular matrix (ECM) environment through Integrins, thus activating signaling pathways that regulate their function. Analysis of our previous RNA sequencing data identified integrin α5 (Itgα5) as one of the most upregulated integrin genes in infarct macrophages. Accordingly, we hypothesized that integrin α5 signaling in infarct macrophages transduces ECM-derived signals, regulating responses critical for repair and remodeling of the infarcted heart. Overall design: In order to study the role of ITGA5 in myeloid cells in vivo, we generated mice with myeloid specific loss of ITGA5 in lysozyme M+ cells (Myα5KO). We used a transgenic mouse line in which Cre recombinase is driven by the LyzM promoter (Jackson Laboratory #004781). LyzM-Cre mice were bred with ITGA5 fl/fl mice (Jackson Laboratory #32299) to generate LyzM-Cre;ITGA5fl/fl animals (Myα5KO) and corresponding ITGA5 fl/fl control littermates. A model of non-reperfused myocardial infarction was induced by permanent ligation of left anterior descending coronary artery in 12-weeks-old mice and samples were collected 7 days after coronary occlusion for ITGA5 fl/fl and Myα5KO. >>> Submitter declares raw data are unavailable and cannot be recovered. <<<