The regulation of membrane 125I- and 86Rb+ permeability in a virally transformed cell line (NCL-SG3) derived from the human sweat gland epithelium
We have explored the factors that may regulate membrane permeability in a cell line (NCL-SG3) derived from the human sweat gland epithelium. Ionomycin increased the rate of 125I-efflux from preloaded cells and this action appeared to be due to an increase in intracellular free calcium ([Ca2+]i). The...
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Veröffentlicht in: | Experimental physiology 1994-05, Vol.79 (3), p.445-459 |
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Zusammenfassung: | We have explored the factors that may regulate membrane permeability in a cell line (NCL-SG3) derived from the human sweat
gland epithelium. Ionomycin increased the rate of 125I-efflux from preloaded cells and this action appeared to be due to an
increase in intracellular free calcium ([Ca2+]i). The ionomycin-evoked increase in 125I- efflux was reduced in cells that
were exposed either to barium or to valinomycin in the presence of a high concentration of external potassium. It thus appears
that a fraction of the ionomycin-evoked increase in 125I- efflux is due to the activation of potassium channels and experiments
using 86Rb+ also suggested that ionomycin increased the rate of potassium efflux, an effect which was totally abolished by
barium. Blockade of Na(+)-K(+)-2Cl- cotransport and of Cl- -HCO3- exchange reduced the basal rate of 125I- efflux and the
ionomycin-evoked increase in 125I-efflux from control cells and from cells depolarized by valinomycin. These transport systems
thus contribute to anion efflux, although [Ca2+]i-dependent chloride channels also appear to be present. Acetylcholine increases
[Ca2+]i in the secretory cells of human sweat glands, but this neurotransmitter did not increase [Ca2+]i in NCL-SG3 cells
and so membrane permeability was not under cholinergic control. Adrenaline did not increase [Ca2+]i, but this hormone did
evoke cyclic-3',5'-adenosine monophosphate (cyclic AMP) production. However, membrane permeability was not under adrenergic
control, as the cells did not appear to express functional, cyclic AMP-dependent anion channels. This may be because they
were not fully differentiated under the culture conditions. ATP consistently evoked a dose-dependent increase in anion efflux
that appeared to be mediated by [Ca2+]i. The increase in [Ca2+]i was initiated by the release of calcium from a limited internal
store and was subsequently sustained by calcium influx. UTP and ADP also increased [Ca2+]i, whereas adenosine, AMP and alpha,beta-methylene
ATP were without effect. These data thus suggest that a subclass of type 2 purine receptor, which is functionally coupled
to phosphoinositidase C, is present in these cells. |
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ISSN: | 0958-0670 1469-445X |
DOI: | 10.1113/expphysiol.1994.sp003779 |