Expression of Inflammation-related Intercellular Adhesion Molecules in Cardiomyocytes In Vitro and Modulation by Pro-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.


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.


CONCLUSIONS
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.
Division 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.
Ibrahim
I
El-Battrawy
First Department of Medicine, Medical Faculty Mannheim, University Heidelberg, Mannheim, Germany German Center for Cardiovascular Research, Partner Site, Heidelberg-Mannheim, Mannheim, Germany.
Erol
E
Tülümen
Division 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.
Siegfried
S
Lang
First Department of Medicine, Medical Faculty Mannheim, University Heidelberg, Mannheim, Germany German Center for Cardiovascular Research, Partner Site, Heidelberg-Mannheim, Mannheim, Germany.
Ibrahim
I
Akin
First Department of Medicine, Medical Faculty Mannheim, University Heidelberg, Mannheim, Germany German Center for Cardiovascular Research, Partner Site, Heidelberg-Mannheim, Mannheim, Germany.
Michael
M
Behnes
Division 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 Institute of Cardiovascular Research, Sichuan Medical University, Luzhou, Sichuan, P.R. China.
Xiabo
X
Zhou
First Department of Medicine, Medical Faculty Mannheim, University Heidelberg, Mannheim, Germany.
Martin
M
Mavany
Institute for Transfusion Medicine and Immunology, Mannheim, Germany.
Peter
P
Bugert
Institute for Transfusion Medicine and Immunology, Mannheim, Germany.
Karen
K
Bieback
First Department of Medicine, Medical Faculty Mannheim, University Heidelberg, Mannheim, Germany German Center for Cardiovascular Research, Partner Site, Heidelberg-Mannheim, Mannheim, Germany.
Martin
M
Borggrefe
First Department of Medicine, Medical Faculty Mannheim, University Heidelberg, Mannheim, Germany German Center for Cardiovascular Research, Partner Site, Heidelberg-Mannheim, Mannheim, Germany.
Elif
E
Elmas
D000199:Actins / Q000378:metabolism; D000328:Adult; D040881:CD11a Antigen / Q000378:metabolism; D039481:CD11b Antigen / Q000378:metabolism; D015815:Cell Adhesion Molecules / Q000378:metabolism*; D002478:Cells, Cultured; D005434:Flow Cytometry; D006801:Humans; D007136:Immunoglobulins / Q000378:metabolism; D007249:Inflammation / Q000378:metabolism; D062745:Junctional Adhesion Molecule A / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008562:Membrane Glycoproteins / Q000378:metabolism; D009088:Mucoproteins / Q000378:metabolism; D032383:Myocytes, Cardiac / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D019007:P-Selectin / Q000378:metabolism; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000378:metabolism; D013917:Thrombin / Q000494:pharmacology*
D000199:Actins; D040881:CD11a Antigen; D039481:CD11b Antigen; D015815:Cell Adhesion Molecules; D007136:Immunoglobulins; D062745:Junctional Adhesion Molecule A; D008070:Lipopolysaccharides; C504265:MADCAM1 protein, human; D008562:Membrane Glycoproteins; D009088:Mucoproteins; D019007:P-Selectin; C084882:P-selectin ligand protein; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D013917:Thrombin
CD31; cardiomyocytes in vitro model; cell adhesion molecules; inflammation