Abstract
Ca 2+ fluxes were examined in HEK 293 cells stably expressing the rat or porcine calcitonin receptors (CTRs). Calcitonin (CT) rapidly increased cytosolic Ca 2+ ([Ca 2+ ] i ) concentrations in these cells in a manner which was sustained in the presence of extracellular Ca 2+ ([Ca 2+] e ). In cells pretreated with CT, elevation of the [Ca 2+ ] e concentration resulted in a further increase in [Ca 2+ ] i which was concentration-dependent with respect to both the concentration of CT and the increment of [Ca 2+ e . Untransfected cells, cells transfected with vector alone, and CTR-transfected cells not treated with CT, were unresponsive to [Ca 2+ ] e . The microsomal Ca 2+ -ATPase inhibitor thapsigargin was able to mimic both the acute [Ca 2+ ] i fluxes and responsiveness to [Ca 2+ ] e mediated by Cr in these cells. The CT-induced responsiveness to [Ca 2+ ] e was neither mimicked by, nor affected by, activators of the cAMP or protein kinase C pathways. Treatment of cells with pertussis toxin influenced neither the primary Ca 2+ fluxes in response to CT or thapsigargin nor the agonist-induced [Ca 2+ ] e influx. Nifedipine failed to block responses to either CT or thapsigargin. These results lead to the important conclusion that the CTR participates in receptor-activated Ca 2+ inflow, in which depletion of intracellular Ca 2+ pools leads secondarily to influx of extracellular Ca2+.
| Original language | English |
|---|---|
| Pages (from-to) | 213-219 |
| Number of pages | 7 |
| Journal | BBA - Molecular Cell Research |
| Volume | 1265 |
| Issue number | 2-3 |
| DOIs | |
| Publication status | Published - 16 Mar 1995 |
| Externally published | Yes |
Keywords
- Calcium influx
- Cloned calcitonin receptor
- Thapsigargin
- Transfected HEK 293 cell
Cite this
}
Calcium inflow in cells transfected with cloned rat and porcine calcitonin receptors. / Findlay, David M.; Houssami, Souheir; Sexton, Patrick M.; Brady, Catherine L.; Martin, T. John; Myers, Damian E.
In: BBA - Molecular Cell Research, Vol. 1265, No. 2-3, 16.03.1995, p. 213-219.Research output: Contribution to journal › Article › Research › peer-review
TY - JOUR
T1 - Calcium inflow in cells transfected with cloned rat and porcine calcitonin receptors
AU - Findlay, David M.
AU - Houssami, Souheir
AU - Sexton, Patrick M.
AU - Brady, Catherine L.
AU - Martin, T. John
AU - Myers, Damian E.
PY - 1995/3/16
Y1 - 1995/3/16
N2 - Ca 2+ fluxes were examined in HEK 293 cells stably expressing the rat or porcine calcitonin receptors (CTRs). Calcitonin (CT) rapidly increased cytosolic Ca 2+ ([Ca 2+ ] i ) concentrations in these cells in a manner which was sustained in the presence of extracellular Ca 2+ ([Ca 2+] e ). In cells pretreated with CT, elevation of the [Ca 2+ ] e concentration resulted in a further increase in [Ca 2+ ] i which was concentration-dependent with respect to both the concentration of CT and the increment of [Ca 2+ e . Untransfected cells, cells transfected with vector alone, and CTR-transfected cells not treated with CT, were unresponsive to [Ca 2+ ] e . The microsomal Ca 2+ -ATPase inhibitor thapsigargin was able to mimic both the acute [Ca 2+ ] i fluxes and responsiveness to [Ca 2+ ] e mediated by Cr in these cells. The CT-induced responsiveness to [Ca 2+ ] e was neither mimicked by, nor affected by, activators of the cAMP or protein kinase C pathways. Treatment of cells with pertussis toxin influenced neither the primary Ca 2+ fluxes in response to CT or thapsigargin nor the agonist-induced [Ca 2+ ] e influx. Nifedipine failed to block responses to either CT or thapsigargin. These results lead to the important conclusion that the CTR participates in receptor-activated Ca 2+ inflow, in which depletion of intracellular Ca 2+ pools leads secondarily to influx of extracellular Ca2+.
AB - Ca 2+ fluxes were examined in HEK 293 cells stably expressing the rat or porcine calcitonin receptors (CTRs). Calcitonin (CT) rapidly increased cytosolic Ca 2+ ([Ca 2+ ] i ) concentrations in these cells in a manner which was sustained in the presence of extracellular Ca 2+ ([Ca 2+] e ). In cells pretreated with CT, elevation of the [Ca 2+ ] e concentration resulted in a further increase in [Ca 2+ ] i which was concentration-dependent with respect to both the concentration of CT and the increment of [Ca 2+ e . Untransfected cells, cells transfected with vector alone, and CTR-transfected cells not treated with CT, were unresponsive to [Ca 2+ ] e . The microsomal Ca 2+ -ATPase inhibitor thapsigargin was able to mimic both the acute [Ca 2+ ] i fluxes and responsiveness to [Ca 2+ ] e mediated by Cr in these cells. The CT-induced responsiveness to [Ca 2+ ] e was neither mimicked by, nor affected by, activators of the cAMP or protein kinase C pathways. Treatment of cells with pertussis toxin influenced neither the primary Ca 2+ fluxes in response to CT or thapsigargin nor the agonist-induced [Ca 2+ ] e influx. Nifedipine failed to block responses to either CT or thapsigargin. These results lead to the important conclusion that the CTR participates in receptor-activated Ca 2+ inflow, in which depletion of intracellular Ca 2+ pools leads secondarily to influx of extracellular Ca2+.
KW - Calcium influx
KW - Cloned calcitonin receptor
KW - Thapsigargin
KW - Transfected HEK 293 cell
UR - http://www.scopus.com/inward/record.url?scp=0028937054&partnerID=8YFLogxK
U2 - 10.1016/0167-4889(94)00229-8
DO - 10.1016/0167-4889(94)00229-8
M3 - Article
C2 - 7696352
AN - SCOPUS:0028937054
VL - 1265
SP - 213
EP - 219
JO - Biochimica et Biophysica Acta - Molecular Cell Research
JF - Biochimica et Biophysica Acta - Molecular Cell Research
SN - 0167-4889
IS - 2-3
ER -