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Methods and Findings
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Methods Find Exp Clin Pharmacol 2000, 22(9): 657
ISSN 0379-0355
Copyright 2000 Clarivate Analytics
CCC: 0379-0355
DOI: 10.1358/mf.2000.22.9.802279
 
 
Investigation into the effects of amyloid (1-42) beta-peptide upon basal and antigen-stimulated hexosaminidase and serotonin release from rat RBL-2H3 basophilic leukemia cells
Englund, P., Jacobsson, S.O.P., Fowler, C.J.
 
 
There is evidence that beta-amyloid (Abeta) peptide infusion in vivo produces a degranulation of vascular mast cells. It would be useful to investigate the interaction between Abeta and mast cells in a simple in vitro model system in order to determine the cellular mechanism by which exposure to Abetapeptides results in mast cell degranulation. In the present study, the effect of Abeta(1-42) upon the release of granular hexosaminidase and serotonin has been investigated using the cognate rat mast cell line, RBL-2H3. Sensitization of these cells for 1 h with anti-DNP IgE (monoclonal anti-dinitrophenyl) results in a large release of hexosaminidase and serotonin due to degranulation when the cells are exposed to DNP-HSA (albumin, human dinitrophenyl). Pretreatment overnight with Abeta(1-42) (10 and 30 mcM) did not affect either the basal or antigen-stimulated release of hexosaminidase or serotonin. A similar lack of effect of Abeta(25-35) and the lipid peroxidation product HNE upon antigen-stimulated release of hexosaminidase or serotonin was also found. It is concluded that RBL-2H3 cells are not a useful model for mechanistic studies into the effects of beta-amyloid peptides upon vascular mast cells.


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