Abstract

Calcitonin, the hypocalcemic hypophosphatemic hormone, is synthesized by the thyroidal C cells in mammals. The sequences of its gene (Jonas et a1.,1985) and the biosynthetic precursor (Jacobs et a1.,1981) is established in rats. In vivo administration of calcium, a potent calcitonin (CT) secretagogue, to rats induces a rapid increase in the translational activity of CT mRNA (Segond et a1.,1984). This rise is coincident with the elevation in plasma CT levels. However total CT mRNA levels as measured by hybridization to a CT specific cDNA probe are unch'*anged up to 30 minutes. We have investigated if CT mRNA levels were modified 1 to 4 hours after Ca administration. CT mRNA was estimated by hybridization and translation. In brief, thyroidal mRNAs were : spotted on GeneScreen membrans, hybridized to a specific CT mRNA probe and CT mRNA measured by quantitative autoradiography. translated in a reticulocyte lysate in the presence of labelled methionine, calcitonln precursor collected by precipitation with specific antibody and quantifified by densitometric scans of autoradiographies of PAGE. Levels of CT mRNA (Table 1) measured by a specific probe increased slowly 30 minutes after the administration of the ion. Th'e translational activity of CT mRNA was roughly parallel to the hybridizable mRNA at all times studied except at 2 minutes after the administration of calcium when the translational activity is almost doubled while the quantities of hybridizable mRNA are not modified. This increased activity of the CT mRNA coincides with the peak of plasma levels of both calcium and CT. Table 1: Change in Calcit0nin mRNA, calcitonin and plasma calcium after acute hypercalcemia.

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