Partial inhibition of SERCA is responsible for extracellular Ca 2+ dependence of AlF4--induced [Ca 2+]i oscillations in rat pancreatic acinar cells

Seon Ah Chong, Soo Young Hong, Seok Jun Moon, Jee Won Park, Jeong Hee Hong, Jeong Mi An, Syng Ill Lee, Dong Min Shin, Jeong Taeg Seo

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4 Citations (Scopus)


AlF4- is known to generate oscillations in intracellular Ca2+ concentration ([Ca2+]i) by activating G proteins in many cell types. However, in rat pancreatic acinar cells, AlF4--evoked [Ca2+]i oscillations were reported to be dependent on extracellular Ca2+, which contrasts with the [Ca2+]i oscillations induced by cholecystokinin (CCK). Therefore, we investigated the mechanisms by which AlF4- generates extracellular Ca2+-dependent [Ca2+]i oscillations in rat pancreatic acinar cells. AlF4--induced [Ca2+]i oscillations were stopped rapidly by the removal of extracellular Ca2+ and were abolished on the addition of 20 mM caffeine and 2 μM thapsigargin, indicating that Ca2+ influx plays a crucial role in maintenance of the oscillations and that an inositol 1,4,5-trisphosphate-sensitive Ca 2+ store is also required. The amount of Ca2+ in the intracellular Ca2+ store was decreased as the AlF4 --induced [Ca2+]i oscillations continued. Measurement of 45Ca2+ influx into isolated microsomes revealed that AlF4- directly inhibited sarco/endoplasmic reticulum Ca2+-ATPase (SERCA). The activity of plasma membrane Ca 2+-ATPase during AlF4- stimulation was not significantly different from that during CCK stimulation. After partial inhibition of SERCA with 1 nM thapsigargin, 20 pM CCK-evoked [Ca 2+]i oscillations were dependent on extracellular Ca 2+. This study shows that AlF4- induces [Ca2+]i oscillations, probably by inositol 1,4,5-trisphosphate production via G protein activation but that these oscillations are strongly dependent on extracellular Ca2+ as a result of the partial inhibition of SERCA.

Original languageEnglish
Pages (from-to)C1142-C1149
JournalAmerican Journal of Physiology - Cell Physiology
Issue number5 54-5
Publication statusPublished - 2003 Nov

All Science Journal Classification (ASJC) codes

  • Physiology
  • Cell Biology


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