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Capsaicin inhibits phospholipase C-mediated Ca(2+) increase by blocking thapsigargin-sensitive store-operated Ca(2+) entry in PC12 cells.

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Authors
Choi, Se-Young; Kim, Kyong-Tai
Issue Date
1999
Publisher
American Society for Pharmacology and Experimental Therapeutics (ASPET)
Citation
Journal of Pharmacology and Experimental Therapeutics 291:107–114
Abstract
Capsaicin has been shown to act through vanilloid receptors,
which are temperature-sensitive cation channels. However,
there also are indications that suggest the capsaicin effect is
not mediated by the vanilloid receptor. We therefore investigated
the effect of capsaicin on the phospholipase C-mediated
Ca21 rise in PC12 cells. Capsaicin caused a rapid decline in
extracellular ATP- or bradykinin-induced calcium transients to
the basal level without significant attenuation of the peak level.
However, capsaicin did not inhibit either ATP- or bradykinininduced
Ca21 elevation in the absence of extracellular Ca21 or
inositol-1,4,5-trisphosphate production. Capsaicin also inhibited
ATP-induced norepinephrine secretion. Capsaicin dramatically
reduced the thapsigargin-induced sustained Ca21 level,
suggesting that capsaicin inhibits thapsigargin-sensitive storeoperated
Ca21 entry (SOCE). Thapsigargin-induced Ba21 and
Mn21 influx was also inhibited by capsaicin. Furthermore, capsaicin
overlapped SK&F96365 in inhibiting thapsigargin-sensitive
SOCE. Capsaicin-induced inhibition of SOCE also occurred
in thapsigargin-treated Jurkat-T cells, which have a
rather prominent SOCE. Resiniferatoxin, a vanilloid receptor
agonist, did not mimic the effect of capsaicin. Ruthenium red
and capsazepine, which are known to inhibit the vanilloid receptor,
did not affect this capsaicin effect. The results suggest
that capsaicin does not mediate vanilloid receptor signaling
when inhibiting the thapsigargin-sensitive SOCE. The capsaicin
action was also not mediated by activation of protein kinase C
because phorbol-12-myristate 13-acetate and capsaicin did
not overlap each other’s effect and GF109203X did not reverse
the inhibitory effect of capsaicin. The results suggest that capsaicin
negatively modulates thapsigargin-sensitive SOCE subsequent
to phospholipase C activation.
ISSN
0022-3565
Language
English
URI
http://hdl.handle.net/10371/58452
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Researcher Institutes (연구소)College of Natural Sciences (자연과학대학)Center for Theoretical Physics(이론물리학연구소)
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