<abstract xmlns="http://www.w3.org/1999/xhtml">

The reduction in mortality following acute myocardial infarction (AMI) is an important achievement of modern medicine. Despite this progress, AMI remains the most common cause of heart failure (HF) and HF-related morbidity and mortality. The involvement of the innate immune response in different stages after AMI has at tracted important attention in recent years. With the increasing range of potential therapeutic compounds and delivery vectors, the need of highly efficient experimental AMI models is increasing, to support further advancement in this field. Here, we present a high-throughput model for the assessment of the innate immune response to AMI. The model is based on permanent surgical ligation of the left descending coronary artery (LAD) in mice, followed by complex flow-cytometry and histological analyses of immune cellular populations in blood and myocardium. We are presenting time-dependent qualitative and quantitative analysis results, demonstrating intense accumulation of Ly6Ghi neutrophils and Ly6Chi monocytes in the infarcted myocardium on days 1 and 3 post-AMI, followed by successive accumulation of reparatory Ly6CloMerTKhi macrophages, neovascularization and fibrosis development by day 7.
</abstract>

The reduction in mortality following acute myocardial infarction (AMI) is an important achievement of modern medicine. Despite this progress, AMI remains the most common cause of heart failure (HF) and HF-related morbidity and mortality. The involvement of the innate immune response in different stages after AMI has at tracted important attention in recent years. With the increasing range of potential therapeutic compounds and delivery vectors, the need of highly efficient experimental AMI models is increasing, to support further advancement in this field. Here, we present a high-throughput model for the assessment of the innate immune response to AMI. The model is based on permanent surgical ligation of the left descending coronary artery (LAD) in mice, followed by complex flow-cytometry and histological analyses of immune cellular populations in blood and myocardium. We are presenting time-dependent qualitative and quantitative analysis results, demonstrating intense accumulation of Ly6Ghi neutrophils and Ly6Chi monocytes in the infarcted myocardium on days 1 and 3 post-AMI, followed by successive accumulation of reparatory Ly6CloMerTKhi macrophages, neovascularization and fibrosis development by day 7.

Studying the Innate Immune Response to Myocardial Infarction in a Highly Efficient Experimental Animal Model

„George Emil Palade” University of Medicine, Pharmacy, Science and Technology

Romanian Journal of Cardiology

This work is licensed under the Creative Commons Attribution 4.0 International License.

The reduction in mortality following acute myocardial infarction (AMI) is an important achievement of modern medicine. Despite this progress, AMI remains the...

Studying the Innate Immune Response to Myocardial Infarction in a Highly Efficient Experimental Animal Model

Article Category: Original Article

Pubblicato online: 05 mag 2022

Pagine: 573 - 585

DOI: https://doi.org/10.47803/rjc.2021.31.3.573

Parole chiave
acute myocardial infarction, experimental model, innate immunity, neutrophils, monocytes, macrophages, myocardial fibrosis, revascularization

© 2021 Razvan Gheorghita Mares et al., published by Sciendo

This work is licensed under the Creative Commons Attribution 4.0 International License.

Studying the Innate Immune Response to Myocardial Infarction in a Highly Efficient Experimental Animal Model

Article Category: Original Article

Pubblicato online: 05 mag 2022

Pagine: 573 - 585

DOI: https://doi.org/10.47803/rjc.2021.31.3.573

Parole chiaveacute myocardial infarction, experimental model, innate immunity, neutrophils, monocytes, macrophages, myocardial fibrosis, revascularization

© 2021 Razvan Gheorghita Mares et al., published by Sciendo

This work is licensed under the Creative Commons Attribution 4.0 International License.

Parole chiave
acute myocardial infarction, experimental model, innate immunity, neutrophils, monocytes, macrophages, myocardial fibrosis, revascularization