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 -