Thromb Haemost 1997; 77(03): 577-584
DOI: 10.1055/s-0038-1656008
Vessel Wall
Schattauer GmbH Stuttgart

Thrombin Augments Vascular Cell-dependent Migration of Human Mast Cells: Role of MGF

Mehrdad Baghestanian
1   The Dept. of Internal Medicine I, Div. of Hematology, The University of Vienna, Austria
,
Roland Hofbauer
2   The Dept. of Anaesthesiology and Gen. Intensive Care Med B, The University of Vienna, Austria
,
Hans G Kress
2   The Dept. of Anaesthesiology and Gen. Intensive Care Med B, The University of Vienna, Austria
,
Johann Wojta
3   The Inst. of Physiology, The University of Vienna, Austria
,
Astrid Fabry
3   The Inst. of Physiology, The University of Vienna, Austria
,
Bernd R Binder
3   The Inst. of Physiology, The University of Vienna, Austria
,
Christoph Kaun
3   The Inst. of Physiology, The University of Vienna, Austria
,
Michael R Müller
4   The Dept. of Surgery II, The University of Vienna, Austria
,
Mohammad R Mehrabi
5   The Dept. of Internal Medicine II, Div. of Cardiology, The University of Vienna, Austria
,
Stylianos Kapiotis
6   The Clinical Inst, of Med. Chem. Lab, The University of Vienna, Austria
,
Gürkan Sengoelge
7   The Department of Internal Medicine III, Div. of Nephrology, The University of Vienna, Austria
,
Minoo Ghannadan
1   The Dept. of Internal Medicine I, Div. of Hematology, The University of Vienna, Austria
,
Klaus Lechner
1   The Dept. of Internal Medicine I, Div. of Hematology, The University of Vienna, Austria
,
Peter Valent
1   The Dept. of Internal Medicine I, Div. of Hematology, The University of Vienna, Austria
› Author Affiliations
Further Information

Publication History

Received 16 July 1996

Accepted after revision 05 November 1996

Publication Date:
26 July 2018 (online)

Summary

Recent data suggest that auricular thrombosis is associated with accumulation of mast cells (MC) in the upper endocardium (where usually no MC reside) and local expression of MGF (mast cell growth factor) (25). In this study, the role of vascular cells, thrombin-activation and MGF, in MC-migration was analyzed. For this purpose, cultured human auricular endocardial cells (HAUEC), umbilical vein endothelial cells (HUVEC) and uterine-(HUTMEC) and skin-derived (HSMEC) microvascular endothelial cells were exposed to thrombin or control medium, and the migration of primary tissue MC (lung, n = 6) and HMC-1 cells (human MC-line) against vascular cells (supernatants) measured. Supernatants (24 h) of unstimulated vascular cells (monolayers of endocardium or endothelium) as well as recombinant (rh) MGF induced a significant migratory response in HMC-1 (control: 3025 ± 344 cells [100 ± 11.4%] vs. MGF, 100 ng/ml: 8806 ± 1019 [291 ± 34%] vs. HAUEC: 9703 ± 1506 [320.8 ± 49.8%] vs. HUTMEC: 8950 ± 1857 [295.9 ± 61.4%] vs. HSMEC: 9965 ± 2018 [329.4 ± 66.7%] vs. HUVEC: 9487 ± 1402 [313.6 ± 46.4%], p <0.05) as well as in primary lung MC. Thrombin-activation (5 U/ml, 12 h) of vascular cells led to an augmentation of the directed migration of MC as well as to a hirudin-sensitive increase in MGF synthesis and release. Moreover, a blocking anti-MGF antibody was found to inhibit MC-migration induced by unstimulated or thrombin-activated vascular cells. Together, these data show that endocardial and other vascular cells can induce migration of human MC. This MC-chemotactic signal of the vasculature is associated with expression and release of MGF, augmentable by thrombin, and may play a role in the pathophysiology of (auricular) thrombosis.

 
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