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Efflux of 45 CA 2+ from human fibroblasts in response to serum or growth factors
Author(s) -
Owen Nancy E.,
Villereal Mitchel L.
Publication year - 1983
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041170105
Subject(s) - efflux , fetal bovine serum , intracellular , chemistry , endocrinology , medicine , amiloride , stimulation , growth factor , ion transporter , biology , receptor , biochemistry , cell , sodium , membrane , organic chemistry
Previous studies have indicated that intracellular Ca 2+ is involved in fetal bovine serum (FBS)‐ or growth factor (GF)‐stimulated Na + influx in human foreskin fibroblasts (HSWP). In the present study, 45 Ca 2+ efflux from serum‐deprived HSWP cells was measured in response to 10% FBS or GF [lys‐bradykinin, vasopressin, epidermal growth factor, and insulin]. Efflux data were analyzed using a computer program and the best fit indicated the presence of three Ca 2+ compartments: a compartment (C 1 ) with a very fast turnover rate, one (C 2 ) with a fast turnover rate, and one (C 3 ) with a slow turnover rate. When serum‐deprived cells were treated with 10% FBS, efflux from C 2 and C 3 increased significantly (p>0.05). Similar effects on efflux were observed when serum‐deprived cells were treated with individual GFs. Combination of the four GFs produced a higher stimulation than any single factor and a response that was equal to that for FBS. On the other hand, when cells were serum‐treated in the presence of the intracellular Ca 2+ antagonist, 8‐(N‐N, diethylamino)‐octyl 3,4,5‐trimethoxybenzoate (TMB‐8), 45 Ca 2+ efflux from C 2 was substantially reduced. Finally, when cells were treated with the Na + transport inhibitor amiloride, there was no significant effect on serum‐stimulated Ca 2+ efflux. These results are consistent with a FBS‐ or GF‐induced mobilization of Ca 2+ that can be blocked by intracellular Ca 2+ antagonists, and support the hypothesis that the action of these agents on Na + influx may be via their effects on intracellular Ca 2+ .