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Updated: Jan 7, 2026
Murine Myocardial Infarction Model using Permanent Ligation of Left Anterior Descending Coronary Artery
Published on: August 16, 2019
Complosome Activation after Myocardial Infarction in a Murine Model of Permanent LAD Ligation
Janina Ratajczak1, Ahmed Abdel-Latif2, Gabriela Schneider1,3
1Stem Cell Institute at James Graham Brown Cancer Center, University of Louisville, 500 S. Floyd Street, Rm. 107, Louisville, KY, 40202, USA.
Insights
The study reveals systemic activation of the Complosome in the heart and hematopoietic tissues following myocardial infarction (MI) in mice. This highlights the intracellular complement cascade's role in stem cell function post-heart attack.
Area of Science:
- Immunology
- Cardiology
- Stem Cell Biology
Background:
- Traditionally, complement cascade (ComC) proteins like C3 and C5 were thought to be solely liver-produced.
- Emerging research indicates complement components are expressed in non-hepatic cells, including cardiomyocytes.
- A novel regulatory pathway, the Complosome, identified in lymphocytes, influences immune responses and metabolism.
Purpose of the Study:
- To investigate the systemic activation of the Complosome in cardiac and hematopoietic tissues after myocardial infarction (MI).
- To differentiate the roles of circulating complement versus intracellular Complosome in stem cell biology and organ injury.
- To explore the potential impact of Complosome expression in stem cells on myocardial infarction outcomes.
Main Methods:
- Utilized a murine model of myocardial infarction (MI).
- Analyzed systemic activation of the Complosome in cardiac and hematopoietic tissues.
- Distinguished between liver-derived circulating complement and intracellular Complosome expression.
Main Results:
- Demonstrated systemic activation of the Complosome in the heart and hematopoietic tissues of mice post-MI.
- Provided evidence for the presence and activation of intracellular complement components within stem cells.
Conclusions:
- The Complosome is systemically activated in cardiac and hematopoietic tissues following myocardial infarction.
- Intracellular complement components (Complosome) may play crucial roles in stem cell survival, growth, differentiation, and trafficking, potentially influencing MI outcomes.
Abstract:
It has been widely accepted for many years that the essential components of the complement cascade (ComC), including C3 and C5 proteins, are produced solely in the liver and released into circulation after synthesis. However, recent evidence shows that complement components are also expressed in other cell types, including human cardiomyocytes. Moreover, a new regulatory loop was identified in lymphocytes that regulates immune responses and metabolism, named the "Complosome." Following this significant discovery, the Complosome has been shown to play a role in the trafficking and metabolism of hematopoietic stem/progenitor cells (HSPCs) and is expressed in several types of bone marrow (BM) resident stem cells. ComC has been studied in various models of tissue and organ injury and regeneration. However, most of these studies did not distinguish between the role of systemic, liver-derived circulating complement in the blood and the complement expressed as a "Complosome" inside cells. Since Complosome is expressed in several types of stem cells that could influence the clinical outcome of myocardial infarction (MI), this distinction is important because intracellular components of the ComC may have beneficial roles in cell survival, growth, differentiation, and trafficking of stem and progenitor cells. We report herein the systemic activation of the Complosome in the heart and hematopoietic tissues in a murine model of myocardial infarction (MI).
