Abstract
Store-operated calcium entry (SOCE) plays an important role in shaping the Ca2+ response of various tissues and cell types. In this report, we show that thapsigargin (TG)-induced SOCE was inhibited by the histamine receptor agonist, histamine-trifluoromethyltoluide (HTMT), in U937 and HL-60 human promyelocytes. Preincubation of HTMT resulted in a significant inhibition of subsequent TG-induced Ca2+ elevation without affecting Ca 2+ release from intracellular stores. HTMT also inhibited TG-induced Ca2+ current and Ba2+/Mn2+ influx in a concentration-dependent manner. In contrast with HTMT, other H1 histamine receptor agonists, histamine, 2-methylhistamine and 2-thiazolylethylamine, did not affect TG-induced SOCE. In addition, HTMT also attenuated TG-induced cytosolic superoxide generation. Taken together, our data clearly suggest that the anti-inflammatory effect of HTMT may occur through direct inhibition of SOCE.
Original language | English (US) |
---|---|
Pages (from-to) | 1613-1622 |
Number of pages | 10 |
Journal | Biochemical Pharmacology |
Volume | 70 |
Issue number | 11 |
DOIs | |
State | Published - Nov 25 2005 |
Externally published | Yes |
Keywords
- Calcium
- HTMT
- Inflammation
- SOCE
- Superoxide
ASJC Scopus subject areas
- Biochemistry
- Pharmacology