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Purinergic agonist ATP is a comitogen in thyroid FRTL‐5 cells
Author(s) -
Törnquist Kid,
Ekokoski Elina,
Dugué Benoit
Publication year - 1996
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/(sici)1097-4652(199602)166:2<241::aid-jcp1>3.0.co;2-p
Subject(s) - pertussis toxin , purinergic receptor , protein kinase c , protein kinase a , biology , extracellular , adenosine triphosphate , kinase , cell growth , stimulation , microbiology and biotechnology , biochemistry , g protein , endocrinology , signal transduction
Several growth factors may stimulate proliferation of thyroid cells. This effect has, in part, been dependent on calcium entry. In the present study using FRTL‐5 cells, we show that in addition to its effect on calcium fluxes, ATP acts as a comitogen in these cells. In medium containing 5% serum, but no TSH, ATP stimulated the incorporation of 3 H‐thymidine in a dose‐ and time‐dependent manner in the cells. At least a 24‐h incubation with ATP was necessary to observe the enhanced (30–50%) incorporation of 3 H‐thymidine and an increased (30%) cell number. The effect of ATP was dependent on insulin in the incubation medium. Furthermore, ATP enhanced the TSH‐mediated incorporation of 3 H‐thymidine. The effect of ATP was apparently mediated via a G‐protein dependent mechanism, as no stimulation of thymidine incorporation was observed in cells treated with pertussis toxin. The effect of ATP was not dependent on the activation of protein kinase C (PKC), as ATP was effective in cells with downregulated PKC. ATP rapidly phosphorylated mitogen activated protein (MAP) kinase in FRTL‐5 cells. In addition, ATP stimulated the expression of a 62 kDa c‐fos dependent protein in a dose‐ and time‐dependent manner. Our results thus suggest that extracellular ATP, in the presence of insulin, may be a cofactor in the regulation of thyroid cell proliferation, probably by phosphorylating MAP kinase and stimulating the expression of c‐fos. © 1996 Wiley‐Liss, Inc.