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Cited by 247

The DOI matches its Crossref record; 15 of the 15 references it cites were found in a registry or an index.

COX-2 Regulates the Insulin-Like Growth Factor I-Induced Potentiation of Zn2+-Toxicity in Primary Cortical Culture

Im, J.-Y.·2004·Molecular Pharmacology
DOI 10.1124/mol.66.3
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Abstract

We have recently found that diethylstilbestrol (DES), a synthetic estrogen agonist, inhibits thrombin-induced Ca(2+) influx in human platelets, but it remains unclear to what extend this effect might be related to the store-operated Ca(2+) influx pathway. To study the effect of DES on store-operated channels and capacitative Ca(2+) influx, we used rat basophilic leukemia (RBL) cells, vascular smooth muscle cells (SMC), and human platelets, and recorded whole-cell Ca(2+) release-activated Ca(2+) (CRAC) currents and thapsigargin (TG)-induced capacitative Ca(2+) influx. In this study, we demonstrate that extracellular DES produces a dose-dependent and reversible inhibition of CRAC currents in RBL cells (IC(50), approximately 0.5 microM), whereas intracellular DES (25 microM) has no effect. Extracellular DES (up to 30 microM) inhibited only CRAC but did not affect a whole-cell monovalent cation current mediated by TRPM7 channels. DES effectively inhibited TG-induced capacitative Ca(2+) influx in a dose-dependent manner with an IC(50) values of approximately 0.1 microM in RBL cells, <0.1 microM in SMC, and approximately 1 microM in human platelets. It is noteworthy that trans-stilbene, a close structural analog of DES that lacks hydroxyl and ethyl groups, had no effect on CRAC current and on store-operated Ca(2+) influx. Thus, we found DES to be a very effective inhibitor of store-operated channels and Ca(2+) influx in a variety of cell types.

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Metadata

Authors
Im, J.-Y.
Venue
Molecular Pharmacology
Publisher
Elsevier BV
Published
2004-09-01
Volume
66
Issue
3
Pages
368-376
ISSN
0026-895X
DOI
10.1124/mol.66.3
OpenAlex
W1863440278
Cited by
247
References
15
FWCI
4.12
Type
journal article
Language
en
Open access
closed

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