A zinc-sensing receptor triggers the release of intracellular Ca2+ and regulates ion transport
AUTOR(ES)
Hershfinkel, Michal
FONTE
The National Academy of Sciences
RESUMO
Changes in extracellular zinc concentration participate in modulating fundamental cellular processes such as proliferation, secretion, and ion transport in a mechanism that is not well understood. Here, we show that a micromolar concentration of extracellular zinc triggers a massive release of calcium from thapsigargin-sensitive intracellular pools in the colonocytic cell line HT29. Calcium release was blocked by a phospholipase-C inhibitor, indicating that formation of inositol 1,4,5-triphosphate is required for zinc-dependent calcium release. Zinc influx was not observed, indicating that extracellular zinc triggered the release. The Cai2+ release was zinc specific and could not be triggered by other heavy metals. Furthermore, zinc failed to activate the Ca2+-sensing receptor heterologously expressed in HEK293 cells. The zinc-induced Cai2+ rise stimulated the activity of the Na+/H+ exchanger in HT29 cells. Our results indicate that a previously uncharacterized extracellular, G protein-coupled, Zn2+-sensing receptor is functional in colonocytes. Because Cai2+ rise is known to regulate key cellular and signal-transduction processes, the zinc-sensing receptor may provide the missing link between extracellular zinc concentration changes and the regulation of cellular processes.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=58801Documentos Relacionados
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