Mast cell-derived VEGF enhances the passage of IgE FE-3 through the rat aortic endothelial cell monolayer.
BACKGROUND
It is well known that the IgE-mediated allergic reaction in various extravascular tissues is induced by the mutual interaction of IgE, target cells (mast cells, MCs) and allergens. However, so far little has been known about the detailed mechanism whereby IgE in the circulating blood is transferred to the extravascular tissue. To examine whether or not MCs are involved in the permeability of IgE across rat aortic endothelial cells (RAECs) in vitro, we determined the permeability constant (PC) of dinitrophenyl-specific rat IgE (IgE FE-3) using a dual chamber system.


METHODS
Isolated RAECs obtained by a primary explant technique were seeded on a collagen-coated membrane in the upper chamber. MCs were collected from the peritoneal cavity of Wistar rats and suspended in the lower chamber. The time-dependent changes in concentration of IgE FE-3 (IgE) in the upper and lower chambers were measured by IgE capture ELISA after addition of IgE (10 microg/ml) to the upper chamber.


RESULTS
The cultured medium of IgE-stimulated MCs significantly increased the PC of IgE (9.86 +/- 0.46 x 10(-6) cm/s), as compared to the value to which calcium ionophore A 23187-stimulated MCs increased the PC of IgE (7.97 +/- 0.21 x 10(-6) cm/s). The increase of PC by IgE-stimulated MCs was most strongly inhibited by suramin (92.3% +/- 1.89), and was weakly inhibited by tranexamic acid, cimetidine and diphenhydramine. In addition, the PC of IgE was increased with the increase in the MC-derived vascular endothelial growth factor/permeability factor (VEGF).


CONCLUSIONS
After IgE is transferred from the circulating blood to the extravascular tissue, it may bind to Fc epsilon RI of the MC and the other Fc epsilon RI-bearing cells. The MC is then activated through the interaction of IgE and Fc epsilon RI. Release of VEGF from the activated MC increases, and the VEGF enhances the permeability of IgE.
Nakasone
Toshiyuki
T
First Department of Physiology, School of Medicine, University of the Ryukyus, 207 Uehara, Nishihara, Okinawa 903-0215, Japan.
Hanashiro
Kazuhiko
K
Nakamura
Mariko
M
Sunakawa
Hajime
H
Kosugi
Tadayoshi
T
D000818:Animals; D001011:Aorta; D015153:Blotting, Western; D000001:Calcimycin / Q000494:pharmacology; D002478:Cells, Cultured; D016228:Endothelial Growth Factors / Q000032:analysis / Q000502:physiology*; D004730:Endothelium, Vascular / Q000166:cytology / Q000378:metabolism*; D007073:Immunoglobulin E / Q000378:metabolism*; D036341:Intercellular Signaling Peptides and Proteins / Q000032:analysis / Q000502:physiology*; D008222:Lymphokines / Q000032:analysis / Q000502:physiology*; D008407:Mast Cells / Q000502:physiology*; D010539:Permeability; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors
D016228:Endothelial Growth Factors; D036341:Intercellular Signaling Peptides and Proteins; D008222:Lymphokines; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors; D007073:Immunoglobulin E; D000001:Calcimycin