Intracellular free calcium concentrations ([Ca++](i)) were studied in polymorphonuclear leukocytes (PMNs) from 13 athyreotic patients who had been previously treated by total thyroidectomy and radioiodine therapy for differentiated thyroid carcinoma, and from age- and sex-matched euthyroid healthy controls. Patients were studied twice, when hypothyroid (visit 1) and after restoration of euthyroidism by L-T-4 TSH-suppressive therapy (visit 2). PMNs from patients at visit I had significantly lower resting [Ca++](i) levels compared to both visit 2 and controls. Values at visit 2 did not differ from those of the controls. Stimulus-induced [Ca++](i) rise was also significantly blunted at visit I and normalized at visit 2, possibly through a differential contribution of distinct intracellular Ca++ stores, as suggested by the response pattern to the chemotactic agent, N-formyl-Met-Leu-Phe (fMLP), to the selective SERCA pump inhibitor, thapsigargine, and to the mitochondrial uncoupler, carbonyl cyanide p-trifluoromethoxyphenyl-hydrazone (FCCP). In vitro treatment of PMNs from healthy subjects with high TSH concentrations impaired intracellular Ca++ store function. Both resting [Ca++] levels and fMLP-induced [Ca++](i) rise increased in the presence either of low-concentration TSH or of T,, but effects of TSH and T-4 were not additive. T-3, rT(3), and TRIAC had no effect. In conclusion, this study provides evidence for a direct relationship between thyroid status and [Ca++](i) homeostasis in human PMNs, mainly related to direct actions of TSH and T-4 on these cells.
Thyroid hormone and thyrotropin regulate intracellular free calcium concentrations in human polymorphonuclear leukocytes: in vivo and in vitro studies
MARINO, FRANCA;GUASTI, LUIGINA;COSENTINO, MARCO;PIANTANIDA, ELIANA ANGELA ROSA;BARTALENA, LUIGI;VENCO, ACHILLE;LECCHINI, SERGIO
2006-01-01
Abstract
Intracellular free calcium concentrations ([Ca++](i)) were studied in polymorphonuclear leukocytes (PMNs) from 13 athyreotic patients who had been previously treated by total thyroidectomy and radioiodine therapy for differentiated thyroid carcinoma, and from age- and sex-matched euthyroid healthy controls. Patients were studied twice, when hypothyroid (visit 1) and after restoration of euthyroidism by L-T-4 TSH-suppressive therapy (visit 2). PMNs from patients at visit I had significantly lower resting [Ca++](i) levels compared to both visit 2 and controls. Values at visit 2 did not differ from those of the controls. Stimulus-induced [Ca++](i) rise was also significantly blunted at visit I and normalized at visit 2, possibly through a differential contribution of distinct intracellular Ca++ stores, as suggested by the response pattern to the chemotactic agent, N-formyl-Met-Leu-Phe (fMLP), to the selective SERCA pump inhibitor, thapsigargine, and to the mitochondrial uncoupler, carbonyl cyanide p-trifluoromethoxyphenyl-hydrazone (FCCP). In vitro treatment of PMNs from healthy subjects with high TSH concentrations impaired intracellular Ca++ store function. Both resting [Ca++] levels and fMLP-induced [Ca++](i) rise increased in the presence either of low-concentration TSH or of T,, but effects of TSH and T-4 were not additive. T-3, rT(3), and TRIAC had no effect. In conclusion, this study provides evidence for a direct relationship between thyroid status and [Ca++](i) homeostasis in human PMNs, mainly related to direct actions of TSH and T-4 on these cells.
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