Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0235290 (bitter taste)
 1,408 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cellular responses of STC-1 cells to two bitter tastants (denatonium and caffeine) were investigated using a calcium-imaging technique and compared with the response to bombesin. Caffeine is known to stimulate taste receptor cells, but the properties of its signaling have not been well studied. STC-1 cells responded to all three molecules in a dose-dependent manner, and when a reverse transcriptase-polymerase chain reaction (RT-PCR) for denatonium receptor was performed, the product of predicted size was detected in STC-1 cells. Furthermore, all three signaling pathways were blocked by a phospholipase C (PLC) inhibitor, demonstrating the essential involvement of PLC in cellular responses. To study the regulatory system of G protein signaling in STC-1 cells, we searched G protein-coupled receptor kinases (GRKs) by the degenerate-primer PCR method and found that GRK2 is expressed. We also demonstrated that three GRKs (GRK2, GRK3 and GRK5) are differentially distributed in the circumvallate papilla while only GRK2 is present in taste bud cells. Finally, we overexpressed GRK2 in SCT-1 cells and found that bombesin-induced response was strongly inhibited by GRK2 but denatonium-activated signaling was not affected. In the case of caffeine, response was decreased by expression of GRK2 only when cells were activated by 1 mM caffeine. Thus, we showed that STC-1 cells emerge as a cell model for studying the molecular mechanism of bitter taste signaling, and could indicate properties of caffeine-induced signaling in comparison with other signaling.
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PMID:Characterization of bitter taste responses of intestinal STC-1 cells. 1574 96

We previously demonstrated the expression of bitter taste receptors of the type 2 family (T2R) and the alpha-subunits of the G protein gustducin (Galpha(gust)) in the rodent gastrointestinal (GI) tract and in GI endocrine cells. In this study, we characterized mechanisms of Ca(2+) fluxes induced by two distinct T2R ligands: denatonium benzoate (DB) and phenylthiocarbamide (PTC), in mouse enteroendocrine cell line STC-1. Both DB and PTC induced a marked increase in intracellular [Ca(2+)] ([Ca(2+)](i)) in a dose- and time-dependent manner. Chelating extracellular Ca(2+) with EGTA blocked the increase in [Ca(2+)](i) induced by either DB or PTC but, in contrast, did not prevent the effect induced by bombesin. Thapsigargin blocked the transient increase in [Ca(2+)](i) induced by bombesin, but did not attenuate the [Ca(2+)](i) increase elicited by DB or PTC. These results indicate that Ca(2+) influx mediates the increase in [Ca(2+)](i) induced by DB and PTC in STC-1 cells. Preincubation with the L-type voltage-sensitive Ca(2+) channel (L-type VSCC) blockers nitrendipine or diltiazem for 30 min inhibited the increase in [Ca(2+)](i) elicited by DB or PTC. Furthermore, exposure to the L-type VSCCs opener BAY K 8644 potentiated the increase in [Ca(2+)](i) induced by DB and PTC. Stimulation with DB also induced a marked increase in the release of cholecystokinin from STC-1 cells, an effect also abrogated by prior exposure to EGTA or L-type VSCC blockers. Collectively, our results demonstrate that bitter tastants increase [Ca(2+)](i) and cholecystokinin release through Ca(2+) influx mediated by the opening of L-type VSCCs in enteroendocrine STC-1 cells.
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PMID:Bitter stimuli induce Ca2+ signaling and CCK release in enteroendocrine STC-1 cells: role of L-type voltage-sensitive Ca2+ channels. 1670 56