P2 purinergic agonists and 12-O-tetradecanoylphorbol-13-acetate, as well as protein kinase A activators, stimulate thyroglobulin secretion in FRTL-5 cells

Biochem Biophys Res Commun. 1993 Mar 15;191(2):385-91. doi: 10.1006/bbrc.1993.1229.

Abstract

We studied the role of various intracellular pathways in thyroglobulin secretion. The P2 agonists (ATP, ADP, GTP), 12-O-tetradecanoylphorbol-13-acetate (TPA), and protein kinase A activators stimulate thyroglobulin secretion in cells grown without TSH. The effects of these agents are additive. Pertussis toxin partially inhibits the effect of ATP but has no effect on the action of GTP. ATP and GTP increase cytosolic calcium (279 +/- 16% and 302 +/- 22%, respectively) while TPA and TSH (1 mU/ml) do not. Thus, both the protein kinase A and kinase C pathways regulate thyroglobulin secretion in FRTL-5 cells.

MeSH terms

  • 8-Bromo Cyclic Adenosine Monophosphate / pharmacology
  • Adenosine Diphosphate / pharmacology
  • Adenosine Triphosphate / pharmacology
  • Cells, Cultured
  • Colforsin / pharmacology
  • Enzyme Activation
  • Guanosine Triphosphate / pharmacology
  • Protein Kinases / metabolism*
  • Receptors, Purinergic / drug effects*
  • Tetradecanoylphorbol Acetate / pharmacology*
  • Thyroglobulin / metabolism*

Substances

  • Receptors, Purinergic
  • Colforsin
  • 8-Bromo Cyclic Adenosine Monophosphate
  • Adenosine Diphosphate
  • Guanosine Triphosphate
  • Adenosine Triphosphate
  • Thyroglobulin
  • Protein Kinases
  • Tetradecanoylphorbol Acetate