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Published on: May 15, 2011
Cellular distribution of angiotensin-converting enzyme after myocardial infarction
M Falkenhahn1, F Franke, R M Bohle
1Department of Pharmacology, University of Kiel, Germany.
Insights
Angiotensin-converting enzyme (ACE) is mainly found in endothelial cells and macrophages after heart attack. Its increased presence during fibrosis suggests a key role in cardiac repair and remodeling.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Tissue Repair Mechanisms
Background:
- Angiotensin-converting enzyme (ACE) plays a critical role in cardiovascular regulation.
- Understanding ACE cellular localization is crucial for studying cardiac remodeling post-myocardial infarction.
- Left ventricular repair involves complex cellular interactions and molecular signaling.
Purpose of the Study:
- To investigate the cellular distribution of ACE in the heart before and after myocardial infarction.
- To identify cell types involved in left ventricular repair and remodeling that express ACE.
- To elucidate the role of ACE in the context of cardiac fibrosis and tissue repair.
Main Methods:
- Immunohistochemical techniques using monoclonal and polyclonal antibodies.
- Analysis of human and rat myocardial tissue samples.
- In situ hybridization for collagen type I in a rat myocardial infarction model.
Main Results:
- In noninfarcted hearts, ACE was primarily in endothelial cells and aortic valve subendocardial layers.
- Post-myocardial infarction, ACE expression was induced in capillary endothelial cells and macrophages at the infarct margin.
- Intense ACE staining was observed in the fibrotic repair zone, inversely correlated with collagen type I expression.
- Vascular smooth muscle cells and cardiomyocytes showed no ACE expression.
Conclusions:
- Endothelial cells are the primary source of ACE expression following myocardial infarction.
- ACE induction during fibrosis suggests a significant role in cardiac tissue repair and remodeling.
- ACE localization patterns provide insights into the molecular mechanisms of post-infarction cardiac healing.
Abstract:
We studied the cellular distribution of angiotensin-converting enzyme (ACE) in the heart related to the cell types involved in left ventricular repair and remodeling before and after myocardial infarction by immunohistochemical techniques using monoclonal and polyclonal antibodies. In noninfarcted myocardium of both human and rat, ACE expression was confined to endothelial cells and subendocardial cell layers of the aortic valve. ACE was prominent in endothelia of small arteries and arterioles, whereas only half the coronary capillaries were immunoreactive and venous vessels were almost completely devoid of the enzyme. In a rat model of myocardial infarction, ACE distribution was determined 1, 3, and 7 days and 2, 3, and 6 weeks after coronary occlusion. Three and 7 days after infarction, endothelial cells of sprouting capillaries and macrophages in the marginal zone of necrosis revealed ACE expression. In both human and rat with the onset of fibrosis, intense staining of the enzyme was found in the marginal zone of the repair tissue. In situ hybridization for collagen type I in the rat revealed that zones with high collagen content had almost no ACE immunoreactivity. Vascular smooth muscle cells and cardiomyocytes revealed no ACE expression throughout the study. We conclude that endothelial cells are the principal source for the expression of ACE after myocardial infarction. The observed induction of ACE with the onset of fibrosis suggests a role of this enzyme that is related to tissue repair and remodeling.
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