Key result
Thyrotrophin and prostaglandin E2 increase cellular cAMP, calmodulin, and phosphodiesterase activity in cultured thyroid cells.
This preclinical study demonstrates that TSH- and PGE2-stimulated increases in calmodulin in porcine thyroid cells are mediated by cAMP, which in turn stimulates cAMP phosphodiesterase.
Should not yet inform thyroid management; hypothesis-generating for cAMP-calmodulin-phosphodiesterase regulation in thyroid cells.
Thyrotrophin (TSH) and prostaglandin E2 (PGE2) increased cellular cyclic AMP (cAMP), calmodulin levels and cAMP phosphodiesterase activity in cultured porcine thyroid cells. Dibutyryl cAMP (dbcAMP), a stable analogue of cAMP, increased calmodulin levels and cAMP phosphodiesterase activity. These results indicate that TSH- and PGE2-stimulated increases in calmodulin are mediated by cAMP. This increased concentration of calmodulin in turn stimulates cAMP phosphodiesterase. Double reciprocal plots of cAMP hydrolysis yielded two apparent Michaelis constants (Km); the lower in the 1 mumol/l and the higher in the 10 mumol/l range. Thyrotrophin, PGE2 and dbcAMP increased the values of maximal velocity without changing the Km values.
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Takasu et al. (1988) studied this question. Thyrotrophin (TSH) and prostaglandin E2 (PGE2) was evaluated on cellular cyclic AMP (cAMP), calmodulin levels and cAMP phosphodiesterase activity. Thyrotrophin and prostaglandin E2 increased cellular cyclic AMP, calmodulin levels, and cAMP phosphodiesterase activity in cultured porcine thyroid cells.
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