Effects of the Chronic and Acute Treatments of Pig Thyroid Cells with Forskolin on the Cyclic AMP Accumulation, the Phospholipid Turnover, and Iodination
Thyrotropin (TSH) exerts its physiological effects on thyroid cells via two pathways. The one involving the stimulation of adenylate cyclase and of cyclic AMP-dependent protein kinase (kinase A) is well documented. The other mechanism is associated with the increased turnover of phosphoinositides and activation of the Ca2+-phospholipid-dependent protein kinase (kinase C). It is very difficult to understand the respective role of both pathways. Until now, the physiological parameters modified by dibutyryl cyclic AMP (iodine metabolism) were considered to be under the control of the cyclic AMP cascade. While it is true that cyclic AMP can regulate the iodination of thyroglobulin, it is difficult to show a regulatory role for the phosphatidylinositol (PI) pathway in this event, because of the absence of partial agonists and antagonists of TSH.
KeywordsAdenylate Cyclase Thyroid Cell Acute Challenge Assay Aliquot Phospholipid Effect
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