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ABSTRACT
Confluent monolayers of cultured porcine thyroid cells transport fluid from the apical to the basal surface, forming circumscribed zones of detachment (domes) from the culture dish substrate. Fluid transport, as measured by increase in dome height, was stimulated by prostaglandin E2 (PGE2; 1 μmol/l) and inhibited by amiloride (0·1–100 μmol/l). Values of the inhibition constant (K i) with 95% confidence limits for each of a series of amiloride analogues were: 3′,4′-dichlorobenzamil (DCB), 0·090 (0·045–0·18) μmol/l; 2′,4′;-dimethylbenzamil (DMB), 0·14 (0·074–0·27) μmol/l; amiloride, 0·72 (0·33–1·8) μmol/l; 5-(N,N-hexamethylene)amiloride (HMA), 17 (5·9–43) μmol/l; 5-(N-ethyl-N-isopropyl)amiloride (EIPA), 33 (15–71) μmol/l; and 2-guanidinobenzimidazole, 243 (110–570) μmol/l. Triaminopyrimidine was ineffective at concentrations up to 1 mmol/l. Since DCB and DMB are known to have a higher affinity for Na+ channels, while HMA and EIPA show higher affinity for Na+/H+ antiports, it was concluded that PGE2-stimulated fluid transport involved an apical membrane Na+ channel.
Journal of Endocrinology (1989) 123, 93–97
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ABSTRACT
Confluent monolayers of cultured porcine thyroid cells transport fluid from the apical to the basal surface, forming circumscribed zones of detachment from the culture dish substrate (domes). The transepithelial potential (TEP), positive on the basal side, was 12·9 ± 0·4 (s.e.m.) mV (n = 93) under control conditions, increasing to 38·9 ± 0·3 mV (n = 281) when fluid transport was stimulated by prostaglandin E2 (PGE2; 1 μmol/l). Forskolin (1 μmol/l) and 8-(4-chlorophenylthio) adenosine 3′,5′-cyclic monophosphate (0·5 mmol/l) were also effective in increasing TEP. Addition of amiloride in concentrations sufficient to block fluid transport (100 μmol/l) reduced the TEP to 5·8 ± 0·3 mV (n=76). Substitution of N-methyl-d-glucamine for sodium in the medium reduced the PGE2-stimulated TEP to 13·4 ± 0·8 mV (n = 32). Substitution of gluconate for chloride increased the TEP to 40·3 ± 0·4 mV (n = 160). Removal of bicarbonate or potassium from the medium, or addition of ouabain (200 μmol/l) were also effective in reducing the TEP. In media of low bicarbonate concentration (1 mmol NaHCO3/l), acetazolamide (1 mmol/l) reduced the TEP. Fluid transport by the monolayer as measured by the change in height of domes was increased by PGE2 (1 μmol/l). PGE2-stimulated fluid transport was inhibited by sodium or chloride ion substitution, bicarbonate removal or the addition of ouabain (200 μmol/l) or amiloride (100 μmol/l). It was concluded that fluid transport in thyroid monolayers is mediated by rheogenic sodium transport with chloride transport being passive, electrogenically coupled to sodium transport. Sodium entry to the apical pole of the cells occurs by an amiloride-sensitive mechanism, and sodium extrusion at the basal pole depends on the Na+/K+ ATPase.
J. Endocr. (1988) 119, 309–314
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ABSTRACT
Thyrotrophin (4-256 μU/ml) promoted an increase in the rate of release of radioiodine from the organic iodine pool of cultured porcine thyroid cells in follicular formations. This action of TSH was antagonized by low concentrations of epidermal growth factor (EGF; 0·1–5 nmol/l). The maximal effect of EGF was reached by 0·5 nmol/l. EGF (0·5–5 nmol/l) also inhibited the stimulatory effect of 8-chloro cyclic AMP (0·06–1·0 nmol/l) on radioiodine turnover. Exposure of thyroid cultures to media with a calcium concentration of 17·7 μmol/l (1% of normal) resulted in a very marked increase in the rate of release of radioiodine. The effect of TSH in low-calcium media was to inhibit the increased release of radioiodine, and EGF (0·5 nmol/l) antagonized this inhibitory effect of TSH. The calcium ionophore, A23187, stimulated radioiodine release in a dose-dependent fashion, and EGF (1·7 nmol/l) inhibited this response. Fluid transport in thyroid monolayers was stimulated by prostaglandin E2 (PGE2; 1 μmol/l). EGF (5 nmol/l) also stimulated fluid transport, but antagonized the effect of PGE2 added subsequently. It was concluded that EGF exerted acute antagonistic effects on thyroid cell responses in vitro to cyclic AMP and agents promoting accumulation of cyclic AMP in time-frames too short for these inhibitory effects to be attributable to the dedifferentiative effect of the growth factor.
Journal of Endocrinology (1991) 128, 213–218
