Related Experiment Video
Updated: Mar 22, 2026
Isolation of Functional Cardiac Immune Cells
Published on: December 5, 2011
Expression of Inflammation-related Intercellular Adhesion Molecules in Cardiomyocytes In Vitro and Modulation by
Ibrahim El-Battrawy1, Erol Tülümen2, Siegfried Lang3
1Division of Experimental Cardiology, Medical Faculty Mannheim, University Heidelberg, Mannheim, Germany First Department of Medicine, Medical Faculty Mannheim, University Heidelberg, Mannheim, Germany German Center for Cardiovascular Research, Partner Site, Heidelberg-Mannheim, Mannheim, Germany Ibrahim.el-battrawy@medma.uni-heidelberg.de.
Insights
Human cardiomyocytes express inflammation-related cell adhesion molecules like CD31. Pro-inflammatory mediators, lipopolysaccharide (LPS) and thrombin, increased CD31 expression but not MADCAM1 or F11R.
Area of Science:
- Cardiovascular Biology
- Immunology
- Cell Biology
Background:
- Cell-surface adhesion molecules are crucial for intercellular processes and leukocyte transmigration during inflammation.
- The expression of these molecules on cardiomyocytes and their response to inflammatory mediators were previously unknown.
Purpose of the Study:
- To investigate the expression of specific cell-adhesion molecules on human cardiomyocytes.
- To determine the effect of pro-inflammatory mediators (thrombin and lipopolysaccharide) on this expression.
Main Methods:
- Primary human cardiomyocyte cultures were treated with thrombin, lipopolysaccharide (LPS), or both.
- Expression of cell adhesion molecules (CD11a, CD11b, CD31, CD62P, CD162, F11 receptor, MADCAM1) was analyzed using flow cytometry.
Main Results:
- Baseline expression was observed for CD31 (22.8%), MADCAM1 (7.1%), and F11R (2.6%) on human cardiomyocytes.
- Thrombin and LPS significantly increased CD31 expression by 26% (p<0.05).
- Neither mediator affected MADCAM1 or F11R expression.
Conclusions:
- Human cardiomyocytes express inflammation-related cell adhesion molecules CD31, MADCAM1, and F11R in vitro.
- Pro-inflammatory mediators LPS and thrombin enhance CD31 expression on cardiomyocytes.
- MADCAM1 and F11R expression on cardiomyocytes remain unaffected by these inflammatory agents.
Background:
Cell-surface adhesion molecules regulate multiple intercellular and intracellular processes and play important roles in inflammation by facilitating leukocyte endothelial transmigration. Whether cardiomyocytes express surface-adhesion molecules related to inflammation and the effect of pro-inflammatory mediators remain unknown.
Materials And Methods:
In the present study, the expression of different cell-adhesion molecules (CD11a, CD11b, CD31, CD62P, CD162, F11 receptor and mucosal vascular addressin cell adhesion molecule 1 (MADCAM1)) and the effect of pro-inflammatory mediators were investigated in an in vitro model of human cardiomyocytes. Cells were supplied as a primary culture of cardiac alpha actin-positive cells from human heart tissue. The cells were incubated for 24 h with 1 U/ml thrombin or 700 ng/ml lipopolysaccharide (LPS) or with a combination of both. The expression of the cell adhesion molecules was measured by flow cytometry.
Results:
In cultured human cardiomyocytes, 22.8% of cells expressed CD31, 7.1% MADCAM1 and 2.6% F11R. CD11a, CD11b, CD62P and CD162 were expressed by fewer than 2% of the cells at baseline. CD31 expression increased on incubation of cardiomyocytes with thrombin by 26% (p<0.05) and with LPS by 26% (p=0.06). The combination of thrombin and LPS did not result in increased levels of CD31 (p>0.10). The pro-inflammatory agents LPS and thrombin had no effect on the expression of MADCAM1 and F11R.
Conclusion:
Inflammation-related cell-adhesion molecules CD31, MADCAM1 and F11R were shown to be expressed on the surface of human cardiomyocytes in an in vitro model. Incubation with LPS or thrombin resulted in increased expression of CD31, however, it did not modify the expression of the cell adhesion molecules MADCAM1 and F11R.
