Two neoplastic human cell lines, WI-38 CT-I and SUSM-I, which were transformed in vitmwith gamma rays and 4 nitroquinoline I oxide, respectively, grew continuously in a serum-free defined medium. The defined medium used was a I:I mixture by volume of Dulbecco's modified
Efflux of 45CA2+ from human fibroblasts in response to serum or growth factors
โ Scribed by Nancy E. Owen; Mitchel L. Villereal
- Publisher
- John Wiley and Sons
- Year
- 1983
- Tongue
- English
- Weight
- 920 KB
- Volume
- 117
- Category
- Article
- ISSN
- 0021-9541
No coin nor oath required. For personal study only.
โฆ Synopsis
Previous studies have indicated that intracellular Ca2+ is involved in fetal bovine serum (FBS)-or growth factor (GF)-stimulated Na+ influx in human foreskin fibroblasts (HSWP). In the present study, 45Ca2+ efflux from serumdeprived HSWP cells was measured in response to 10% FBS or GF [lysbradykinin, vasopressin, epidermal growth factor, and insulin]. Efflux data were analyzed using a computer program and the best fit indicated the presence of three Ca2+ compartments: a compartment (C3) with a very fast turnover rate, one (C,) with a fast turnover rate, and one (C,) with a slow turnover rate. When serum-deprived cells were treated with 10% FBS, efflux from C2 and C3 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 Ca2+ antagonist, 8-(N-N,diethylamino)-octyl-3,4,5-trimethoxybenzoate (TMB-8), 45Ca2+ efflux from C2 was substantially reduced. Finally, when cells were treated with the Na+ transport inhibitor amiloride, there was no significant effect on serum-stimulated Ca2+ efflux. These results are consistent with a FBS-or GF-induced mobilization of Ca2+ that can be blocked by intracellular Ca2+ antagonists, and support the hypothesis that the action of these agents on Na+ influx may be via their effects on intracellular Ca2+
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