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| 3: Cell Signal. 2003 Jul;15(7):689-697. |
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- Histamine potentiates IP(3)-mediated Ca(2+) release via
thapsigargin -sensitive Ca(2+) pumps.
Aguilar-Maldonado B, Gomez-Viquez L, Garci;a L, Del Angel RM, Arias-Montano
JA, Guerrero-Hernandez A.
Departamento de Bioqui;mica, CINVESTAV-IPN, Apdo. Postal 14-740, D.F. 07000,
Mexico, Mexico
We have studied the histamine-induced potentiation of inositol
1,4,5-trisphosphate (IP(3))-mediated Ca(2+) release in HeLa cells.
Intracellular IP(3) levels were increased by IP(3) dialysis with the
whole-cell configuration of the patch-clamp technique (cell dialysis of
IP(3)). Low concentrations of extracellular histamine (1 &mgr;M) accelerated
the rate of IP(3)-mediated Ca(2+) release, an effect that required the
coincidence of both histamine signalling and the increase in IP(3) levels. Our
data suggest that the potentiation effect of histamine cannot be explained
simply by agonist-induced increase in IP(3) levels. Disordering microfilaments
with cytochalasin D and microtubules with colchicine caused a decrease in the
histamine-induced Ca(2+) response. Furthermore, both cytochalasin D and
colchicine diminished the rate of IP(3)-mediated Ca(2+) release, while only
the former reduced slightly the histamine-induced potentiation effect.
Remarkably, rapid inhibition of SERCA pumps with thapsigargin to avoid the
depletion of internal Ca(2+) stores diminished the histamine-induced
potentiation of IP(3)-mediated Ca(2+) release, without affecting the rate of
IP(3)-mediated Ca(2+) release. These data indicate that histamine-induced
potentiation of Ca(2+) release in HeLa cells requires active SERCA pumps and
suggest that SERCA pumps are an important factor in determining the efficiency
of agonist-induced Ca(2+) release.
PMID: 12742229 [PubMed - as supplied by publisher]
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