The Journal of Experimental Medicine
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Published online 18 September 2000.
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© The Rockefeller University Press, 0022-1007/2000/9/801/ $5.00
The Journal of Experimental Medicine, Volume 192, Number 6, September 18, 2000 801-812

Original Article

Human Endothelial Cells Regulate Survival and Proliferation of Human Mast Cells

Claudia T. Mierkea, Matthias Ballmaierc, Uwe Wernerb, Michael P. Mannsa, Karl Weltec, and Stephan C. Bischoffa

a Department of Gastroenterology and Hepatology, Medical School Hannover, D-30625 Hannover, Germany
b Department of Visceral and Transplant Surgery, Medical School Hannover, D-30625 Hannover, Germany
c Department of Pediatric Hematology and Oncology, Medical School Hannover, D-30625 Hannover, Germany
Department of Gastroenterology and Hepatology, Medical School Hannover, Carl-Neuberg Street 1, D-30625 Hannover, Germany.49-511-532-489649-511-532-8489

bischoff.stephan{at}mh-hannover.de

Mast cells (MCs) are immunoregulatory and inflammatory tissue cells preferentially located around blood vessels. Since endothelial cells have been suggested to regulate MC functions, we analyzed MC–endothelial cell interactions in vitro by performing coculture experiments with purified human intestinal MCs and human umbilical vein endothelial cells (HUVECs). We found that HUVECs provide signals allowing MCs to survive for at least 3 wk and to proliferate without addition of cytokines; otherwise all MCs died. HUVEC-dependent MC proliferation was more pronounced than that induced by stem cell factor (SCF), known to act as an MC growth factor both in vitro and in vivo. After coculture with HUVECs, most MCs were of the tryptase and chymase double-positive phenotype (MCTC). Transwell experiments suggested that the HUVECs' effects on MCs are not mediated by soluble factors. HUVEC-dependent MC adhesion and proliferation were inhibited by neutralizing antibodies directed against SCF and vascular cell adhesion molecule (VCAM)-1 expressed on HUVECs, and c-kit and very late antigen 4 (VLA-4) on MCs. The data suggest that two mechanisms (membrane-bound SCF/c-kit and VCAM-1/VLA-4) are involved in human MC–endothelial cell interactions. In conclusion, our study provides evidence that endothelial cells regulate MC survival and preferentially support human MCTC development.

Key Words: adhesion • fibroblast • integrins • intestinal mucosa • stem cell factor

Abbreviations used in this paper: BrdU, 5-bromo-2'-deoxyuridine; FB, fibroblast; HUVEC, human umbilical vein endothelial cell; ICAM, intracellular adhesion molecule; MC, mast cell; MCT, tryptase-positive MC(s); MCTC, tryptase and chymase double-positive MC(s); mSCF, membrane-bound SCF; SCF, stem cell factor; sSCF, soluble SCF; VCAM, vascular adhesion molecule; VLA-4, very late antigen 4.

© 2000 The Rockefeller University Press


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