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Updated: May 21, 2026
Imaging Cleared Embryonic and Postnatal Hearts at Single-cell Resolution
Published on: October 7, 2016
Cellular immunophenotypes in human embryonic, fetal and adult heart
Alina Grigore1, D Arsene, Fl Filipoiu
1Department of Pathology, Victor Babes National Institute of Pathology, Bucharest, Romania.
Insights
Investigating cardiac cells, this study reveals dynamic immunoprofiles in normal and ischemic hearts. Myofibroblasts, not fibroblasts, drive ischemic remodeling, with altered cell markers during development and disease.
Area of Science:
- Cardiovascular Biology
- Immunohistochemistry
- Cardiac Pathophysiology
Background:
- The cellular immunoprofile of cardiac dysfunction, particularly ischemic lesions, is poorly understood, especially the role of non-cardiomyocytes.
- Existing research lacks detailed insights into the dynamic changes in cellular markers during cardiac development and ischemic injury.
Purpose of the Study:
- To elucidate the immunoprofile of cardiac cells, including cardiomyocytes and non-cardiomyocytes, in embryonic, fetal, and adult normal or ischemic myocardium.
- To identify the cellular origins of myofibroblasts involved in ischemic cardiac remodeling.
Main Methods:
- Immunohistochemistry was employed on myocardial tissue samples from embryonic, fetal, and adult stages, encompassing both normal and ischemic conditions.
- Expression patterns of key markers such as smooth muscle alpha-actin, DDR2, vimentin, CD34, and EGFR were analyzed.
Main Results:
- Smooth muscle alpha-actin expression decreased from embryonic to fetal stages, was absent in adult cardiomyocytes, but prominent in ischemic fibrotic scars.
- DDR2 and vimentin, present in early cardiac cells, were absent in fibrotic scar tissue, suggesting myofibroblast involvement in ischemic remodeling.
- An increased EGFR-positive vascular network in ischemic hearts points to a potential role in cardiac pre- and post-conditioning.
Conclusions:
- Cardiomyocytes and non-cardiomyocytes exhibit significant immunoprofile variations across developmental stages and in response to ischemic injury.
- Myofibroblasts, characterized by smooth muscle alpha-actin and CD34 expression, are the primary cellular contributors to fibrotic scar formation in ischemic cardiomyopathy.
- The EGFR pathway may play a crucial role in the adaptive responses of the ischemic heart.
Abstract:
The cellular immunoprofile of cardiac dysfunctions and lesions of ischemic etiology are insufficiently studied to date, especially regarding the contribution of non-cardiomyocytic structures. Aiming to explore this immunoprofile, we used immunohistochemistry applied on embryonic, fetal and adult normal or ischemic myocardium. We observed a decrease of smooth muscle alpha-actin expression in fetal vs. embryonic cardiomyocytes, its absence in normal adult myocardium and its intense expression in the fibrotic scars of ischemic myocardium. DDR2 and vimentin, which are present in the interstitial cells and cardiomyocytes of the embryo, fetus and normal adult heart, are absent in the fibrotic scar tissue and cicatricial infarction, the latter expressing smooth muscle alpha-actin and CD34. This suggested that myofibroblasts and not local fibroblasts that participate in ischemic remodeling. An EGFR-positive vascular network was better represented in the ischemic heart than in the adult normal one, a fact possibly related to EGFR implication in cardiac ischemic pre- and post-conditioning. Therefore, cardiomyocytes and non-cardiomyocytic cells have an undulating immunoprofile according to the intrauterine life stage or age after birth, and a variable contribution in cardiac lesions, mostly in ischemic ones.
