The expression of the 35- and 67-kDa calcimedins is dependent on thyroid hormone.

We have investigated the expression of the 35- and 67-kDa calcimedins and calmodulin during fetal and neonatal periods and in adulthood in rat liver, muscle, and brain. The 35- and 67-kDa calcimedin expression in liver and muscle increased during the perinatal period and correlated with the thyroid status of the developing rat. In fact, animals treated with thyroxine demonstrated a precocious appearance of the 35- and 67-kDa calcimedin in liver and muscle. Animals treated with methylthiouracil, an inhibitor of T4 and T3 synthesis, strongly suppressed the synthesis of the calcimedins in these tissues. Neither treatment influenced the levels of either the 35- and 67-kDa calcimedins in brain. In contrast, each tissue examined produced a unique pattern of calmodulin expression during development. None of the tissue calmodulin concentrations changed during hyper- or hypothyroid states. Collectively, these data support the concept that the intracellular calcium signal possesses multiple, independent molecular pathways of mediation. In addition, the variety of these pathways is influenced by hormonal preconditioning in that the cellular response to elevated cytosolic calcium is dependent upon the thyroid status of a tissue.