Thapsigargin

 
3: Cell Signal. 2003 Jul;15(7):689-697.  
 
 
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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