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, DongMin Shin, Jeong Taeg Seo

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

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
JournalAmerican Journal of Physiology - Cell Physiology
Volume285
Issue number5 54-5
Publication statusPublished - 2003 Nov 1

Fingerprint

Sarcoplasmic Reticulum Calcium-Transporting ATPases
Acinar Cells
Cholecystokinin
Inositol 1,4,5-Trisphosphate
Thapsigargin
GTP-Binding Proteins
tetrafluoroaluminate
Microsomes
Caffeine
Adenosine Triphosphatases
Maintenance
Cell Membrane

All Science Journal Classification (ASJC) codes

  • Physiology
  • Cell Biology

Cite this

Chong, Seon Ah ; Hong, Soo Young ; Moon, Seok Jun ; Park, Jee Won ; Hong, Jeong Hee ; An, Jeong Mi ; Lee, Syng Ill ; Shin, DongMin ; Seo, Jeong Taeg. / Partial inhibition of SERCA is responsible for extracellular Ca 2+ dependence of AlF4--induced [Ca 2+]i oscillations in rat pancreatic acinar cells. In: American Journal of Physiology - Cell Physiology. 2003 ; Vol. 285, No. 5 54-5.
@article{c613ca98724b438399560909f4b9f560,
title = "Partial inhibition of SERCA is responsible for extracellular Ca 2+ dependence of AlF4--induced [Ca 2+]i oscillations in rat pancreatic acinar cells",
abstract = "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.",
author = "Chong, {Seon Ah} and Hong, {Soo Young} and Moon, {Seok Jun} and Park, {Jee Won} and Hong, {Jeong Hee} and An, {Jeong Mi} and Lee, {Syng Ill} and DongMin Shin and Seo, {Jeong Taeg}",
year = "2003",
month = "11",
day = "1",
language = "English",
volume = "285",
journal = "American Journal of Physiology",
issn = "0363-6143",
publisher = "American Physiological Society",
number = "5 54-5",

}

Partial inhibition of SERCA is responsible for extracellular Ca 2+ dependence of AlF4--induced [Ca 2+]i oscillations in rat pancreatic acinar cells. / Chong, Seon Ah; Hong, Soo Young; Moon, Seok Jun; Park, Jee Won; Hong, Jeong Hee; An, Jeong Mi; Lee, Syng Ill; Shin, DongMin; Seo, Jeong Taeg.

In: American Journal of Physiology - Cell Physiology, Vol. 285, No. 5 54-5, 01.11.2003.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Partial inhibition of SERCA is responsible for extracellular Ca 2+ dependence of AlF4--induced [Ca 2+]i oscillations in rat pancreatic acinar cells

AU - Chong, Seon Ah

AU - Hong, Soo Young

AU - Moon, Seok Jun

AU - Park, Jee Won

AU - Hong, Jeong Hee

AU - An, Jeong Mi

AU - Lee, Syng Ill

AU - Shin, DongMin

AU - Seo, Jeong Taeg

PY - 2003/11/1

Y1 - 2003/11/1

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=0142052908&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0142052908&partnerID=8YFLogxK

M3 - Article

C2 - 12878491

AN - SCOPUS:0142052908

VL - 285

JO - American Journal of Physiology

JF - American Journal of Physiology

SN - 0363-6143

IS - 5 54-5

ER -