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TOPICAL COLLECTIONS

Methods to Investigate Cycling, Proliferation, and Lineage Tracing of Multiple Cell Types in Transgenic Models After Myocardial Infarction

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Matthew Wolf

Matthew Wolf

University of Virginia

Dr. Wolf is an Associate Professor of Medicine in the Division of Cardiology and a resident faculty member of the Robert M. Berne Cardiovascular Research Center (CVRC) at the University of Virginia. He serves as the Co-Director of the Cardiovascular Genetics Clinic and Associate Program Director of the Cardiology Fellowship Program at UVA. His research interests include animal models of cardiomyopathies and myocardial infarction. His early research developed the use of Optical Coherence Tomography (OCT) to measure cardiac chamber size and function in Drosophila melanogaster for large genetic screens of cardiomyopathy genes. His laboratory has recently focused on transgenic mouse models of cardiac disease to investigate cardiac physiology and cellular responses to injury, particularly ischemia-reperfusion myocardial infarction. His research group recently developed new lineage-tracing mice to identify adult cardiomyocytes that reenter the cell cycle after injury. Dr. Wolf is a Fellow of the American Heart Association and a member of the American Society of Clinical Investigation.

Collection Overview

Recent advances in transgenic technologies have provided new opportunities to investigate the cellular and molecular responses to myocardial infarction and cardiac injuries more thoroughly. Lineage tracing experiments can identify and quantify the contributions of multiple cell types during wound healing in the heart. For example, pre-existing cardiac endothelial cells are critical to angiogenesis after myocardial infarction. Resident cardiac fibroblasts become myofibroblasts during infarct development. Specific macrophage subtypes influence fibroblast responses and the extracellular matrix to orchestrate scar formation. Endogenously cycling cardiomyocytes proliferate and endoreplicate after cardiac injury.

In addition to labeling specific cell populations, transgenic methods that manipulate genes by restricted expression of Cre recombinases have uncovered new understandings of how signals control monocytes and macrophages, fibroblasts, endothelial cells, and cardiomyocytes to contribute collectively to wound healing in the context of myocardial infarction and cardiac injury. More recent advances in CRISPR-mediated gene editing have also elucidated how genes and pathways contribute to the wound healing response to myocardial infarction.

Fundamental to all these investigations are the methods to produce reproducible myocardial injuries and measure tissue and organ responses, paramount necessities to interpret the biological processes. This Methods Collection aims to provide various state-of-the-art techniques and tools that use animal models of myocardial infarction and injury, particularly in the context of transgenics.

Articles

An Intact Pericardium Ischemic Rodent Model
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An Intact Pericardium Ischemic Rodent Model

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Cited by 5

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2021

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