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Updated: Jun 25, 2026
On-Chip Endothelial Inflammatory Phenotyping
Published on: July 21, 2012
Regulation of cardiomyocyte full-length tissue factor expression and microparticle release under inflammatory
S Antoniak1, U Boltzen, A Eisenreich
1Department of Cardiology and Pneumology, CharitéCentrum 11 - Herz-, Kreislauf- und Gefässmedizin, Charité- Universitätsmedizin Berlin, Campus Benjamin Franklin, Berlin, Germany.
Summary Background:
Myocardial inflammation is associated with an increase in circulating microparticles (MPs) and procoagulability.
Objectives:
We determined whether acute inflammation was associated with altered full-length tissue factor (flTF) expression and increased procoagulability in cardiomyocytic cells.
Methods:
This study examined the transcriptional regulation of flTF expression in murine cardiomyocytic (HL-1) cells. Also, the generation of MPs by HL-1 cells and their ability to diffuse through an artificial endothelium was evaluated.
Results:
Constitutive and tumor necrosis factor-alpha (TNF-alpha)-induced flTF expression of HL-1 was reduced when c-Jun N-terminal kinase (JNK) was inhibited. Tissue factor (TF)-positive procoagulant MPs were released from HL-1 cells in response to TNF-alpha. JNK inhibition potentiated the release of MPs from HL-1 cells without affecting MP-associated TF activity. MP generation was dependent on RhoA activation and associated with a reorganization of the actin cytoskeleton. Increased diffusion of HL-1-derived MPs through an endothelial monolayer was found after TNF-alpha treatment. The increased diffusion was dependent not only on TNF-alpha but also on HL-1-released mediators.
Conclusions:
Full-length TF expression in HL-1 cells was regulated through JNK. The TNF-alpha-induced increase in procoagulability was mediated through RhoA-dependent release of flTF-bearing MPs. These MPs were able to diffuse through an endothelial barrier adjacent to HL-1 cells and increased the procoagulability of the extracellular endothelial space. Cardiomyocytes seem to be a likely source of flTF-bearing procoagulant MPs.
