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Characterization of Functional Vanilloid Receptors Expressed by Mast
Cells
Tamás Bíró,
Marcus Maurer,
Shayan Modarres,
Nancy E. Lewin,
Chaya Brodie,
Géza Ács,
Péter Ács,
Ralf Paus, and
Peter M. Blumberg
From the Molecular Mechanisms of Tumor Promotion Section, Laboratory
of Cellular Carcinogenesis and Tumor Promotion, National Cancer
Institute, National Institutes of Health, Bethesda, MD; and the
Department of Dermatology, Charité, Humboldt Universität zu
Berlin, Berlin, Germany.
Capsaicin and its ultrapotent analog resiniferatoxin (RTX) act
through specific vanilloid receptors on sensory neurons. The C-type
receptor is coupled to 45Ca uptake, whereas the R-type is
detectable by [3H]RTX binding. We describe here specific
vanilloid responses in murine mast cells (MCs). In the MC lines and in
bone marrow-derived mast cells, capsaicin and RTX induced
45Ca uptake similarly to that observed for cultured rat
dorsal root ganglion neurons (DRGs). This response was antagonized by
the antagonists capsazepine and ruthenium red. As in DRGs, pretreatment of MCs with capsaicin or RTX induced desensitization to subsequent stimulation of 45Ca uptake. The potency for desensitization
by RTX in the MCs corresponded to that for 45Ca uptake,
whereas in DRGs it occurred at significantly lower concentrations
corresponding to that for the high-affinity [3H]RTX
binding site. Consistent with this difference, in MCs we were unable to
detect [3H]RTX binding. Vanilloids were noncytotoxic to
the MCs, in contrast to the DRGs. Although vanilloids did not cause
degranulation in MCs, in the P815 clone capsaicin evoked selective
interleukin-4 release. We conclude that certain MCs possess vanilloid
receptors, but only the C-type that functions as a channel. Our finding
that MCs can respond directly to capsaicin necessitates a reevaluation of the in vivo pathway of inflammation in response to vanilloids.
Blood, Vol. 91 No. 4 (February 15), 1998:
pp. 1332-1340
© 1998 by The American Society of Hematology.
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