作者: Ching-Jiunn Tseng , Chung-Ren Jan
DOI:
关键词: Endoplasmic reticulum 、 Phospholipase 、 Endocrinology 、 Chemistry 、 Phospholipase C 、 Thapsigargin 、 Aristolochic acid 、 Molecular biology 、 Phospholipase A2 、 Internal medicine 、 Phospholipase D 、 Activator (genetics)
摘要: The effect of 3-[1-( p -chlorobenzyl)-5-(isopropyl)-3- tert -butylthioindol-2-yl]-2, 2-dimethylpropanoic acid (MK-886), a leukotriene biosynthesis inhibitor, on Ca2+ mobilization in Madin- Darby canine kidney cells has been examined by fluorimetry using fura-2 as indicator. MK-886 at 0.5 to 25 μM concentration dependently increased [Ca2+]i. [Ca2+]i increase comprised an immediate initial rise and slowly decaying phase. removal inhibited the signals reducing both decay phase, suggesting that activated influx release. In Ca2+-free medium, 10 still after pretreatment with carbonylcyanide m -chlorophenylhydrazone (CCCP; 2 μM), mitochondrial uncoupler, thapsigargin (1 endoplasmic reticulum pump inhibitor. Conversely, abolished CCCP- thapsigargin-induced Ca2+release. This suggests released Ca2+from reticulum, mitochondria, other stores. addition 3 mM for 700 s indicating induced capacitative entry. entry was partly SKF96365 (50 econazole (25 inhibiting phospholipase A2with aristolochic (40 μM) but not D 0.1 propranolol. (10 μM)-induced Ca2+release altered C U73122 (2 50% suppressing A2 propranolol (0.1 mM) respectively.